# Question
Title: How do neurons decide how to alter their output signals?
In computer science, neural networks are trained using backpropagation and other methods. Backpropagation heavily relies on mathematical formulas to describe how the weights should be changed throughout the network to effect the final output of the system. Biological neurons need to be able to adjust as well, if I'm not mistaken. What happens within a neuron to cause it to adjust its output? In other words, are biological neurons "trained" and if so, what is the process behind it?

# Answer
This will be a long post. FYI.

To my knowledge, there is no evidence for back propagation in the brain. If you're interested specifically in that topic, Geoffrey Hinton (Dept. of CS @ UofT) has written about it. I'll try to focus on the biology.

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Some basic neurophysiology first. Neurons have a slightly negative electrical resting potential (prototypically ~-70 mV). When they fire (following *depolarization*) this increases. As you may guess, they can also *hyperpolarize* (less potential to fire an impulse). As you may also be able to guess, other neurons in the network can influence one another to make them more or less likely to fire. This, and indeed most, neuron-neuron communication occurs at synapses. A synapse is a small gap between the presynaptic neuron and postsynaptic neuron, as you're likely already aware. Respectively, these correspond to an axon (sending a signal) and a dendrite (receiving a signal). Long story short, when depolarized the presynaptic neuron releases neurotransmitters (NT) which are received by the post synaptic neuron. This results in changes in concentration of ions in the postsynaptic neuron (inside vs. outside of the neuron). This can result in the postsynaptic neuron firing itself. The ions primarily implicated in this are Sodium (Na+) and Potassium (K+), transduced though ion specific Na+ and K+ ion channels in neuronal membranes.

One of the most critical ions related to your question, however, is Calcium (specifically, Ca2+). This ion often acts as an intracellular messenger, that is when it is 'let into' the cell after that neuron receives an impulse, it activates biochemical processes inside the neuron, e.g., to produce more of a protein.

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How neurons actually learn has been a difficult problem to model. We know that neurons can potentate, that is a neuron can come to exert more control over the firing of another neuron. Indeed, it has been known for a long time that firing neurons strengthen connections. The famous aphorism for this is "neurons that fire together, wire together" (coined by the brilliant scientist Carla Shatz, now at Stanford). The problem is that if neurons just kept getting stronger, it leaves no room for information to be 'unlearned', which it is obvious it can be, for new information to be added to the system, or, indeed, information to ever be really learned at all. You'll see why in a moment.

One attempt to model the problem of neuronal learning is **Beinenstock Cooper and Munro (BCM) Theory**. Its basic proposition is that a connection that was once weak can become strong (and *vica versa*). Specifically, what it attempts to model can be thought of as follows:

Imagine we have three stimuli (e.g., red, green, blue) and three cells. Before much exposure, all of these neurons respond ~equally to each of the stimuli (colors). After exposure the neurons respond differentially, that is neuron 1 might respond strongest to red; neuron 2 to green; and neuron 3 to blue. We might call this 'learning' because we wittness an increase in responding to a stimuli but also -- and this is critical -- a *decrease* in responding to other stimuli.

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Biologically, one heavily implicated mechanism in this process is the N-methyl-D-aspartate receptor (NMDAR). Following binding of glutamate (a NT), this receptor allows Ca2+ into the postsynaptic cell. This animates intracellular events that result in either potentiation (typically in the form of Long Term Potnetation \[LTP\]) or depression (typically in the form of Long Term Depression \[LTD\]). In short, an increase or decrease a presynaptic neurons' ability to exert control over the postsynaptic neuron.

In simple terms:

```
> When low amounts of Ca2+ are conducted through the NMDAR --> LTD
> When hight amounts of Ca2+ are conducted through the NMDAR --> LTP

```

Critically, there is a modification threshold. This is the point at which LTD turns into LTP. This is represented by the greek letter theta (θ). BCM theory proposes a shifting threshold. If a synapse gets very strong, then θ shifts such that it becomes difficult to strengthen the connection further and *easier* to weaken it. Likewise, if a synapse becomes very depressed, θ will shift to allow it to more easily become potentiated and harder to weaken it.

For example, graphically you can visualize potentiation as the threshold shifting to the right. That is, the amount of Ca2+ that would have produced potentiation, now produces depression. The reverse, obviously, can also happen.

---

As you can see, what we've arrived at is something that looks rather computational. While I am not aware of a *truly* precise mathematical description of this process, it is obvious that such a description is, in principle, possible. You can see the math. proposed currently here (it seems implausible it could be that simple to me...and the assumptions made seem daft, but that's just my own commentary). There are precise models of neuronal potentials and people are trying to put BCM (or something like it) into very precise terms. As you can image, this is extremely difficult because of the complexity of the biology, especially what Ca2+ is actually doing in the cell. In many ways, that is still a black box although we're learning about it at a very rapid rate.

In closing, biology seems to have solved the problem of learning very differently than computer scientists. As someone with both a mathematics and neuroscience background, I find the fact that this is possible to be simply incredible.
> 8 votes

# Answer
**Short answer**
Neurons can increase or decrease the amplitude of their response. A neuron's response strength can be regulated by adjustment of the cell-surface expression of excitatory receptors.

**Background**
First off, this question is very broad. To narrow it down I will focus on learning processes in the *hippocampus* involving long-term potentiation (LTP). LTP in the hippocampus is thought to be an essential feature of learning. Much of the work on LTP has focused on the synaptic connections between the Schaffer collaterals and CA1 pyramidal cells (Fig. 1).

Fig. 1. LTP in hippocampus. Source: Purves *et al*. (2001).

Electrical stimulation of Schaffer collaterals generates excitatory postsynaptic potentials (EPSPs) in the postsynaptic CA1 cells (Figure 1). If the Schaffer collaterals are stimulated only two or three times per minute, the size of the evoked EPSP in the CA1 neurons remains constant. However, a brief, high-frequency train of stimuli (a **tetanic stimulation**) to the same axons causes **LTP**, which is evident as a long-lasting **increase in EPSP amplitude** (Fig. 2). LTP also occurs at many other synapses, both within the hippocampus and in a variety of other brain regions, including the cortex, amygdala, and cerebellum (Purves *et al*., 2001).

Fig. 2. LTP. Long-term potentiation of Schaffer collateral-CA1 synapses. (A) Recording of synaptic transmission. Two stimulating electrodes (1 and 2) activate Schaffer collaterals. (B) Left: Synaptic responses recorded in a CA1 neuron in response to single stimuli of synaptic pathway 1, minutes before and one hour after a high-frequency train of stimuli. The high- frequency stimulus train increases the size of the EPSP evoked by a single stimulus. Right: Responses produced by stimulating synaptic pathway 2, which did not receive high-frequency stimulation, is unchanged. (C) The time course of changes in the amplitude of EPSPs evoked by stimulation of pathways 1 and 2. High-frequency stimulation of pathway 1 causes a prolonged enhancement of the EPSPs in this pathway (purple). This potentiation of synaptic transmission in pathway 1 persists for several hours, while the amplitude of EPSPs produced by pathway 2 (orange) remains constant. Source: (Purves *et al*., 2001).

For LTP to occur, both pre- and postsynaptic neurons need to be active at the same time, because the postsynaptic neuron must be depolarized when glutamate is released presynaptically. This has to with the need to overcome the Mg2+ block of NMDAR receptors. NMDA receptors are regulatory receptors that allow Ca2+ to enter the cell. Ca2+, in turn, can affect important regulatory processes in neurons, such as receptor expression. As a consequence of coincident depolarization and glutamate binding, calcium influx (through NMDARs) is maximal, which activates intracellular signaling cascades that ultimately are responsible for the altered synaptic efficacy. NMDAR-dependent LTP is therefore an associative form of plasticity and fulfills the criteria for correlated activity.

Conversely, long-term depression can be induced by repeated activation of the presynaptic neuron at low frequencies without postsynaptic activity. Because the driving force for Ca2+ is very large for a neuron at rest and the block of NMDARs by Mg2+ is incomplete even at resting potentials, significant Ca2+ enters the cell in response to synaptic stimulation during low-frequency synaptic stimulation. Presumably it is repeated occurrence of this smaller NMDAR-dependent Ca2+ influx that triggers LTD induction (Lüscher & Malenka, 2012).

While NMDA receptors are key to learning, it is the workhorse of glutamatergic signalling that ultimately mediates LTP, namely the AMPA receptor. LTP is generally thought to be mediated by an **increase of AMPA receptors** in the postsynaptic neuron, conversely, LTD uis believed to be mediated by a decrease in expressed AMPA receptors. The process of AMPA receptor shuttling between intracellular vesicles and the cell membrane takes only minutes (Malinow, 2003).

**References**
**-** Lüscher & Malenka, *Perspect Biol* (2012); **4**(6): a005710
**-** Malinow, *Philos Trans R Soc Lond B Biol Sci* (2003); **358**(1432): 707–14
**-** Purves *et al*. eds. *Neuroscience*. 2nd ed. Sunderland (MA): Sinauer Associates; 2001
> 5 votes

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Tags: neuroscience, learning, neurophysiology
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# Question
Title: Is there a correlation between high IQ and creativity?
Is there a correlation between high IQ for example over 125 and creativity?

Is creativity improved or does its importance simply diminish?

Maybe there could also be confounding variables as well? It can be easier to be creative if you're not the best in the world in something (surprisingly enough), since then it might motivate you to get off the beaten path.

# Answer
> 22 votes
The article The Threshold Theory Regarding Creativity and Intelligence: An Empirical Test with Gifted and Nongifted Children found results that do not support this "Threshold Theory" of creativity.

Abstract:

> Results of divergent thinking tests (administered to 228 intermediate school students, of whom about 43 percent were gifted) and calculated correlations between creativity and intelligence measures did not support the threshold theory which posits that creativity and intelligence are related only up to an intelligence quotient of about 120.

Can Only Intelligent People Be Creative? A Meta-Analysis by Kyung Hee Kim found a negligible correlation of IQ and creativity and does not support the Threshold Theory.

> The mean correlation coefficient was small (r = .174; 95% CI = .165 – .183), but heterogeneous; this correlation coefficient indicates that the relationship between creativity test scores and IQ scores is negligible. Age contributed to the relationship between intelligence and creativity the most; different creativity tests contributed to it secondly. This study does not support threshold theory.

Several studies dispute the claims of Threshold Theory but the most interesting is probably Biochemical Support for the “Threshold” Theory of Creativity: A Magnetic Resonance Spectroscopy Study which appears to show some support for the idea in a fairly rigorous biochemical method.

There is at best contentious support for the threshold theory, and perhaps more importantly the association between creativity and IQ seems rather weak.

# Answer
> 5 votes
Although the idea that IQ only enables creativity "up to IQ 120" is widespread (and repeated in pop-psych books such as those of Gladwell etc.), large scale studies of giftedness reliably find that the IQ and creativity are associated even at the very highest-extremes of ability. IQ is linearly related to creative achievement across the range (Wai et al., 2005).

A reanalysis by Silvia (2008) of the Wallach and Kogan (1965) paper which originated the idea of a 120 IQ "threshold" found that the original data do not sustain the idea of a critical level.

The suggestion above by @BenBrocka that creativity and IQ are not linked (or only weakly associated) is not supported by the weight of evidence. Nusbaum & Silvia (2011), for instance show that IQ accounts for around 40% of creativity.

**Refs**

Nusbaum, E. C., & Silvia, P. J. (2011). Are intelligence and creativity really so different?: Fluid intelligence, executive processes, and strategy use in divergent thinking. Intelligence, 39(1), 36-45. pdf

Silvia, Paul J. (2008) Creativity and intelligence revisited: A latent variable analysis of Wallach and Kogan (1965). *Creativity Research Journal* **20**. 34-39. pdf.

Wai, J., Lubinski, D., & Benbow, C. P. (2005). Creativity and occupational accomplishments among intellectually precocious youths: an age 13 to age 33 longitudinal study. *Journal of Educational Psychology*, **97**, 484. pdf

# Answer
> 3 votes
There is an update regarding the debate on Threshold Theory. From Jauk et al (2013) "The relationship between intelligence and creativity: New support for the threshold hypothesis by means of empirical breakpoint detection":

> One of the most prominent notions concerning the interplay between intelligence and creativity is the threshold hypothesis, which assumes that above-average intelligence represents a necessary condition for high-level creativity. ... The threshold hypothesis is commonly investigated by splitting a sample at a given threshold (e.g., at 120 IQ points) and estimating separate correlations for lower and upper IQ ranges. However, there is no compelling reason why the threshold should be fixed at an IQ of 120, and to date, no attempts have been made to detect the threshold empirically. ... Segmented regression allows for the detection of a threshold in continuous data by means of iterative computational algorithms. We found thresholds only for measures of creative potential but not for creative achievement. For the former the thresholds varied as a function of criteria: When investigating a liberal criterion of ideational originality (i.e., two original ideas), a threshold was detected at around 100 IQ points. In contrast, a threshold of 120 IQ points emerged when the criterion was more demanding (i.e., many original ideas). Moreover, an IQ of around 85 IQ points was found to form the threshold for a purely quantitative measure of creative potential (i.e., ideational fluency). These results confirm the threshold hypothesis for qualitative indicators of creative potential and may explain some of the observed discrepancies in previous research.

# Answer
> 0 votes
Generally, there is poor support for the threshold theory. Though the last poster referenced a newer study which applied 'empirical break-point detection', such results are unsurprising, because of their tautological nature. The results depend on a specific definition of what creativity is, and only then could the authors obtain a relationship. Furthermore, any relationship between creativity and IQ, is likely better explained by the mediation of specific sub-factors, for example long term memory fluency, complex fluency, and associative memory. Creativity is left best as being defined as, the ability to produce novel relationships. The threshold theory, is just a means for intelligentsia (analytical proponents) to inflate the value of IQ, and maintain their elitist and grandiose sense of worth.

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Tags: measurement, intelligence, iq, creativity, correlation
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# Question
Title: Intentionally making ourselves remember things that never happened
I've been reading an interesting book which makes mostly founded claims. However, there is no reference to any studies in regards to one of the following claims: according to the author, visualizing something that never happened every day for 3 weeks results in a memory which seems as real as any memory of something that did happen

Let's not focus on the 3 weeks statement. The interesting part is the claim that we can actually create memories which are as good as real. I am well aware that our memory is terrible. I've read around about various ways in which our memories can be changed: phrasing questions in a certain way, basing some false information on real information, priming etc.

But can we *really* make something that behaves just like a real memory, even if we are well aware that in reality, it's just a scenario that we imagined and repeated in our minds multiple times?

# Answer
If I understood correctly, you are talking about "false memories" in the context of the following definition in (Johnson, M. K., 2001)

> "A false memory is a mental experience that is mistakenly taken to be a veridical representation of an event from one's personal past. Memories can be false in relatively minor ways (e.g., believing one last saw the keys in the kitchen when they were in the living room) and in major ways that have profound implications for oneself and others (e.g., mistakenly believing one is the originator of an idea or that one was sexually abused as a child)."

From Scientific American, September 1997, Vol. 277 # 3, pages 70-75

This is a an article from 1997 by Elizabeth Loftus that may shed light on your question. Yes, the information may be outdated and recent research might have expanded on it. **In that case, I might edit my answer soon to reflect those updates after completing further readings relating to the topic**

If recent developments interest you, in a study published in the journal *Science*, Tonegawa et. al \[associated with RIKEN-MIT Center for Neural Circuit Genetics\] manipulated individual neurons to manipulate encoded memories in the brains of mice. Read here.

**Misinformation Effect**

> My own research into memory distortion goes back to the early 1970s, when I began studies of the "misinformation effect." These studies show that when people who witness an event are later exposed to new and misleading information about it, their recollections often become distorted. In one example, participants viewed a simulated automobile accident at an intersection with a stop sign. After the viewing, half the participants received a suggestion that the traffic sign was a yield sign. When asked later what traffic sign they remembered seeing at the intersection, those who had been given the suggestion tended to claim that they had seen a yield sign. Those who had not received the phony information were much more accurate in their recollection of the traffic sign.
>
> My students and I have now conducted more than 200 experiments involving over 20,000 individuals that document how exposure to misinformation induces memory distortion. In these studies, people "recalled" a conspicuous barn in a bucolic scene that contained no buildings at all, broken glass and tape recorders that were not in the scenes they viewed, a white instead of a blue vehicle in a crime scene, and Minnie Mouse when they actually saw Mickey Mouse. Taken together, these studies show that misinformation can change an individual's recollection in predictable and sometimes very powerful ways.

**False Childhood Memories**

> My research associate, Jacqueline E. Pickrell, and I settled on trying to plant a specific memory of being lost in a shopping mall or large department store at about the age of five. Here's how we did it. We asked our subjects, 24 individuals ranging in age from 18 to 53, to try to remember childhood events that had been recounted to us by a parent, an older sibling or another close relative. We prepared a booklet for each participant containing one-paragraph stories about three events that had actually happened to him or her and one that had not. We constructed the false event using information about a plausible shopping trip provided by a relative, who also verified that the participant had not in fact been lost at about the age of five. The lost-in-the-mall scenario included the following elements: lost for an extended period, crying, aid and comfort by an elderly woman and, finally, reunion with the family.
>
> After reading each story in the booklet, the participants wrote what they remembered about the event. If they did not remember it, they were instructed to write, "I do not remember this." In two follow-up interviews, we told the participants that we were interested in examining how much detail they could remember and how their memories compared with those of their relative. The event paragraphs were not read to them verbatim, but rather parts were provided as retrieval cues. The participants recalled something about 49 of the 72 true events (68 percent) immediately after the initial reading of the booklet and also in each of the two follow-up interviews. After reading the booklet, seven of the 24 participants (29 percent) remembered either partially or fully the false event constructed for them, and in the two follow-up interviews six participants (25 percent) continued to claim that they remembered the fictitious event. Statistically, there were some differences between the true memories and the false ones: participants used more words to describe the true memories, and they rated the true memories as being somewhat more clear. But if an onlooker were to observe many of our participants describe an event, it would be difficult indeed to tell whether the account was of a true or a false memory. Of course, being lost, however frightening, is not the same as being abused. But the lost-in-the-mall study is not about real experiences of being lost; it is about planting false memories of being lost. The paradigm shows a way of instilling false memories and takes a step toward allowing us to understand how this might happen in real-world settings. Moreover, the study provides evidence that people can be led to remember their past in different ways, and they can even be coaxed into "remembering" entire events that never happened.

**Imagination Inflation**

> What happens when people imagine childhood experiences that did not happen to them? Does imagining a childhood event increase confidence that it occurred? To explore this, we designed a three-stage procedure. We first asked individuals to indicate the likelihood that certain events happened to them during their childhood. The list contains 40 events, each rated on a scale ranging from "definitely did not happen" to "definitely did happen." Two weeks later we asked the participants to imagine that they had experienced some of these events. Different subjects were asked to imagine different events. Sometime later the participants again were asked to respond to the original list of 40 childhood events, indicating how likely it was that these events actually happened to them. Consider one of the imagination exercises. Participants are told to imagine playing inside at home after school, hearing a strange noise outside, running toward the window, tripping, falling, reaching out and breaking the window with their hand. In addition, we asked participants questions such as "What did you trip on? How did you feel?" In one study 24 percent of the participants who imagined the broken-window scenario later reported an increase in confidence that the event had occurred, whereas only 12 percent of those who were not asked to imagine the incident reported an increase in the likelihood that it had taken place. We found this "imagination inflation" effect in each of the eight events that participants were asked to imagine. A number of possible explanations come to mind. An obvious one is that an act of imagination simply makes the event seem more familiar and that familiarity is mistakenly related to childhood memories rather than to the act of imagination. Such source confusion when a person does not remember the source of information can be especially acute for the distant experiences of childhood.

**Impossible Memories**

> A procedure for planting "impossible" memories about experiences that occur shortly after birth has been developed by the late Nicholas Spanos and his collaborators at Carleton University. Individuals are led to believe that they have well-coordinated eye movements and visual exploration skills probably because they were born in hospitals that hung swinging, colored mobiles over infant cribs. To confirm whether they had such an experience, half the participants are hypnotized, age-regressed to the day after birth and asked what they remembered. The other half of the group participates in a "guided mnemonic restructuring" procedure that uses age regression as well as active encouragement to re-create the infant experiences by imagining them.. Spanos and his co-workers found that the vast majority of their subjects were susceptible to these memory-planting procedures. Both the hypnotic and guided participants reported infant memories. Surprisingly, the guided group did so somewhat more (95 versus 70 percent). Both groups remembered the colored mobile at a relatively high rate (56 percent of the guided group and 46 percent of the hypnotic subjects). Many participants who did not remember the mobile did recall other things, such as doctors, nurses, bright lights, cribs and masks. Also, in both groups, of those who reported memories of infancy, 49 percent felt that they were real memories, as opposed to 16 percent who claimed that they were merely fantasies. These findings confirm earlier studies that many individuals can be led to construct complex, vivid and detailed false memories via a rather simple procedure. Hypnosis clearly is not necessary.

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**Sources:**

The formation of false memories.
Loftus, E. F. & Pickrell, J. E. (1995).
*Psychiatric Annals*, 25, 720-725.

Imagination Inflation: Imagining A Childhood Event Inflates Confidence That It Occurred.
Maryanne Carry, Charles G. Manning, Elizabeth F. Loftus and Steven J. Sherman
*Psychonomic Bulletin and Review*, Vol. 3, No. 2, pages 208-214; June 1996.

Remembering Our Past: Studies In Autobiographical Memory.
Edited by David C. Rubin.
*Cambridge University Press*, 1996.

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**Additional Reading:**

Crisis or Creation: A systematic examination of false memory claims.
Dallam, S. (2002).
*Journal of Child Sexual Abuse* 9 (3/4): 9–36.

False Memories Affect Behavior.
*Association for Psychological Science* (2008, August 20).

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> 7 votes

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Tags: memory, long-term-memory, visualization
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# Question
Title: Why is memory selective in storing sometimes irrelevant details and discarding important things?
This has happened many times: I recall unimportant details and forget the important things.

Everyone will recognize this for sure, for example when studying topography, you know which number accompanied the city, but you can't recall its place on the map during the exam, or you can remember which chapter and section number the question is explained in, but you dont't know the answer. You might forget what the main topic of a YouTube video is, but remember what the guy who was talking in the video looked like, or forget where you left off when working on the computer, but remember a time when Microsoft Word auto-corrected spelling.

My question is: **Why is memory selective in storing sometimes irrelevant details and discarding important things**?

# Answer
> 4 votes
There could be several reasons, I'm sure. One particular explanation that sticks out to me is a concept called 'feature integration theory'. I mention this because the things you say you remember -- what the guy in a video looked like, a time when your spelling was auto-corrected, general mundane details or 'features' -- are in line with this theory. You might find this document helpful, but as it is rather long, I'll provide a shorter explanation.

> Feature integration theory is a theory of attention developed in 1980 by Anne Treisman and Garry Gelade that suggests that when perceiving a stimulus, features are "registered early, automatically, and in parallel, while objects are identified separately" and at a later stage in processing.

In other words, our perception of features are quicker and more automatic, registered early on. The object itself is recognized later, and thus we do not always fully integrate it into our attention. We must provide ourselves enough time to integrate the features that we have perceived into one main object or idea, and if we shift our attention away during this mandatory time of attention, we will not recognize the object as one larger entity or idea, but rather a collection of the features that we noticed automatically. This also might explain why you retain less information while multi-tasking.

> Treisman distinguishes between two kinds of visual search tasks, "feature search" and "conjunction search". Feature searches can be performed fast and pre-attentively for targets defined by only one feature, such as color, shape, perceived direction of lighting, movement, or orientation. Features should "pop out" during search and should be able to form illusory conjunctions. Conversely, conjunction searches occur with the combination of two or more features and are identified serially. Conjunction search is much slower than feature search and requires conscious attention and effort. In multiple experiments, some referenced in this article, Treisman concluded that color, orientation, and intensity are features for which feature searches may be performed.

Indeed, this theory is supported by the existence of Balint's syndrome \[1\], a not-quite-understood condition in which damage to the parietal lobe renders the patient with a variety of symptoms, including simultanagnosia, or the 'inability to perceive simultaneous events or objects in one's visual field.'

> This spatial disorder of visual attention—the ability to identify local elements of a scene, but not the global whole—has been referred to as a constriction of the individual's global gestalt window—their visual "window" of attention. People fixate their eyes to specific images in social scenes because they are informative to the meaning of the scene. Any forthcoming recovery in simultanagnosia may be related to somehow expanding the restricted attentional window that characterizes this disorder.
>
> Simultanagnosia is a profound visual deficit. It impairs the ability to perceive multiple items in a visual display, while preserving the ability to recognize single objects. One study suggests that simultanagnosia may result from an extreme form of competition between objects which makes it difficult for attention to be disengaged from an object once it has been selected. Patients with simultanagnosia have a restricted spatial window of visual attention and cannot see more than one object at a time. They see their world in a patchy, spotty manner. Therefore, they pick out a single object, or even components of an individual object, without being able to see the global "big picture."

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Sources:

\[1\] Udesen H, Madsen AL (May 1992). "\[Balint's syndrome--visual disorientation\]". Ugeskr. Laeg. (in Danish) 154 (21): 1492–4.

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Tags: memory, long-term-memory, short-term-memory, semantic-memory
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# Question
Title: What is the role of Chloride (Cl- ions) in membrane potential?
This Membrane Potential article mentions only that Cl- ion is used to model inhibitory GABA synapses. Does it have another role besides hyper-polarizing the cell due to inhibitory neurotransmitter binding?

For example, Cl- ions are not taken into consideration in the Pinsky & Rinzel 1994 Model or in Pospischil et. al. 2008 Models.

# Answer
In normal neurons, Chloride's reversal potential is near the resting potential for the neuron and also happens to be near the leak conductance reversal potential for the neuron. While not exactly the same these three are sometimes confused.

The difference between these three reversal potentials is subtle.

* Chloride Reversal Potential: is the potential carried only by the chloride ion. Therefore it given by the Nernst Equilibrium Potential.
* Leak Reversal Potential: The conductance that remains (relatively) constant. As useful metaphor the leak conductance is the passive conductance of ions through the membrane. This current can be carried by any Ion.
* Resting Potential: The voltage where the neuron is at rest, usually when it is at a steady state. It is defined by all ion's that permeate the membrane at rest. (see GHK)

Because these three reversal potentials are approximately the same that means many computational neuroscience papers will consider only consider the leak current like the two paper's you linked. However, if there is reason to consider Chloride conducting channels specifically (like GABA receptors) then there will be a specific term for the Chloride Ion's Reversal potential.

From a computational perspective, the fact that the Chloride reversal potential is close to the rest potential is actually important. It is capable of shunting inhibition. In short this means that the neurons membrane potential is moved closer to rest, rather than more negative as is the case with regular hyperpolarizing current carried by Potassium Ions. Thus if the membrane potential is below the driving potential for chlorine the shunting inhibition will actually slightly depolarize the cell. Note that this small depolarization will not pass the chlorine reversal potential, thus keeping the cell at rest and preventing firing, despite "depolarizing the cell"

While it is generally true that hyperpolarizing current suppresses firing, there are exceptions to this rule. For example, if a neuron is a resonator (fires in response to certain frequency of input) then hyperpolarizing inputs at the right frequency will cause the neuron to fire. Note, However this is only true for the current carried by Potassium Ions, and shunting inhibition will prevent this type of hyperpolarize-induced firing. The reasoning for this is quite complex, but a good (albeit math-heavy) explanation see Dr. Izhikevich's book Chp 7.
> 3 votes

# Answer
**Short answer**
Mostly Cl- is disregarded in calculations of the resting membrane potential and action potential voltage changes, because it is less important for the neural membrane characteristics than Na+ and K+.

**Background**
In some neurons Cl- is not actively transported. In terms of the resting membrane potential, Cl- hence settles its gradient passively across the membrane according to its Nernst potential, as it has a relatively large permeability in most neurons. The Nernst potential of Cl- is hence governed by the concentration and voltage gradients of Na+ and K+. Na+ and K+ are actively transported out and into the cell, respectively, by the action of the Na+,-K+-ATPase (the sodium potassium pump).

The Nernst potential of Cl- can be calculated with the Nernst equation:

However, many neurons have a K+/Cl- co-transporter that uses the K+ gradient to push Cl- against its concentration gradient out of the cell. In this case there is more Cl- outside the cell than there would be without the active transport. Hence, opening of Cl- channels as in your GABAA example, will hyperpolarize the cell because Cl- will enter upon Cl- channel opening. Secondary active transport of Cl- may also affect the resting membrane potential of these neurons as it will actively participate in the overall membrane potential when actively transported. When taking into account the relative permeabilities of K+, Na+ and Cl-, i.e., 1 : 0.04 : 0.5, the Goldman equation can be used to calculate the membrane potential:

**Reference**
**-** Kandel *et al*. eds. *Principles of Neural Science*, 4th ed. McGraw-Hill, 2000
> 3 votes

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Tags: neuroscience, computational-modeling, electrophysiology
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# Question
Title: Are action potentials necessary for experience?
We know that, for example, during brain surgery, electrical stimulation in certain parts of the cortex is sufficient for experience, and result in reportable experiences in human subjects.

We also know that action potentials are not sufficient to cause experience when they occur in other parts of the body. For example, as far as I know, humans are not aware of action-potential-caused insulin release in the pancreatic cells.

Further we know that mechanical stimulation of the fingers is converted to action potential trains, then relayed via interneurons, and is subsequently reported as touch. The situation is similar with other senses.

But, are there any examples of reportable experience without preceding action potentials? In other words, **are there any cases of experience that is not correlated with electrical activity?**

I'm interested because my deeper question is "Does all qualia result from action potentials?"

# Answer
It is generally accepted that *all activity having to do with conscious experience is mediated by spiking* in the cortex. Sub-threshold activity, such as excitatory postsynaptic potentials (EPSPs) are not carried forward in the nervous system and will 'fade' before having an effect. It all revolves around action potentials.

Quoting from Kandel *et al.* (2000):

> Action potentials constitute the signals by which the brain receives, analyzes and conveys information. These signals are **highly stereotyped** throughout the nervous system \[...\]. The information conveyed by the action potentials is determined not by the form of the signal but by the pathway the signal travels. The brain analyzes *patterns* of incoming electrical signals and in this way ***creates our everyday sensations*** of sight, touch, taste, smell, and sound.

**Reference**
Kandel *et al*. eds. *Principles of Neural Science*, 4th ed. McGraw-Hill, 2000
> 5 votes

# Answer
I think it is safe to say that we simply don't understand nearly enough (anything?) about the neural basis of qualia / experience to be able to give a satisfying answer to this question. That said, at least in the case of human experience, most neuroscientists would agree that if there is any centralized locus of experience it is the brain, and although the brain does have some non-action-potential "commerce", a great deal of it is through action potential mediated communication; I would find it hard to believe that it wasn't involved in conscious experience.

More importantly, being able to test whether one could be consciously experiencing while silencing 100% of action potentials seems like a rather tough experiment to do, given that doing that would probably kill the subject (such as with tetrodotoxin poisoning).
> 2 votes

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Tags: neuroscience, cognitive-neuroscience, philosophy-of-mind
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# Question
Title: Strengthened Inhibitory Connections Between Neurons
I'm reading Bio Inspired Artificial Intelligence which cites this passage about neuron plasticity:

> "Spike time-dependent plasticity. The percentage of synaptic modification depends on the difference between presynaptic and postsynaptic spikes (tpre −tpost). The temporal difference in the figure ranges between -100 ms and +100 ms. When the postsynaptic neuron fires after arrival of the presynaptic pulse (positive difference, also known as causal relation), the synaptic weight is increased; instead, when the postsynaptic neuron fires before the arrival of the presynaptic pulse (negative differ- ence, also known as anticausal difference), the synaptic weight is depressed." From Gerstner and Kistler (2002) plotted on data from Bi and Poo (2001).

How do inhibitory neurons, which have successfully inhibited an activation spike of a neuron, strengthen their connections with such neurons, as the neurons they stop don't spike?

# Answer
The learning rule you describe (i.e. the change of synaptic weights from source neuron to target neuron depending on the temporal difference between source and target activity) is often referred to as 'classical' or 'standard' STDP (spike-timing dependent plasticity) and is focused on connections between excitatory cells. However, this simple form of plasticity is not enough to explain all experimental observations and has also computational problems with respect to stability i.e. there is in fact no 'standard' STDP, because the weight change is not only dependent on the temporal difference, but also on the voltage, location of the synapse, firing rate, the cell-type and probably other factors, see e.g. this article from 2010 dealing with questions surrounding STDP by Lisman and Spruston.

In short, the form of the learning rule depends on several factors and synaptic plasticity works differently for inhibitory cells. As the question as to how plasticity works involving inhibitory cells is not an easy topic, I will refer to this review paper which deals with different induction protocols and potential functional implications (e.g. stability, homeostasis): Review paper on inhibitory synaptic plasticity by Vogels et al.

Very recently, there also has been a research topic in Frontiers of Cellular Neuroscience on this topic: The editorial article briefly summarizes the different contributions
> 6 votes

# Answer
**Short answer**
The question is kind of broad, and I decided to give four notable examples from credible sources of long-term potentiation of inhibitory responses (iLTP) below. Upregulation of postsynaptic GABAA and GABAB currents are the predominant effectors responsible for iLTP. The mechanism through which these effects are initiated are, however, variable between the various systems described. As far as I can see, non of the examples are Hebbian (i.e., non of the examples below are dependent on spike-timing).

**Background**
Repetitive firing of interneurons has been shown to enhance the spike-mediated inhibitory postsynaptic currents in **CA1 pyramidal neurons in the hippocampus**. this enhancement was mediated by *GABAB receptors*. The hippocampus is a brain structure where most of the research in long-term potentiation has been done in the past decades. It is a hot spot of learning and synaptic plasticiy where long-term potentiation is *also induced by repetitive (tetanic) stimulation*. The enhanced inhibitory responses were mediated by *astrocytes* that in turn affected the inhibitory responses in the pyramidal neurons. Astrocytes may therefore be a necessary intermediary in activity-dependent modulation of inhibitory synapses in the hippocampus. The mechanism through which the glial cells did this was not described in the paper. It was *not* mediated via Cl- or K+ (Kang *et al*., 1998).

In **hippocampal neurons** it has been shown that prolonged depolarization of cultured cells leads to *increased expression of inhibitory GABAA receptors* that ultimately decrease the artificially-induced high spike rate activity to normal levels (Rannals & Kapur, 2011). This increase in GABAA activity was accompanied by a larger activity of GABA syntheszing enzyme *GAD*, likely showing increased GABA release.

In the **thalamus**, postsynaptic *thalamocortical (TC) cells* show inhibitory long-term potentiation (iLTP). This iLTP was explicitly shown to be **non-Hebbian**, because it did not depend on the timing between presynaptic and postsynaptic activity. Instead, it was shown to be induced by postsynaptic burst activity alone. iLTP required postsynaptic dendritic Ca2+ influx that triggered the synthesis of nitric oxide that retrogradely activated presynaptic guanylyl cyclase, in turn resulting in the presynaptic expression of iLTP (Sieber *et al*., 2013).

A last example of iLTP was described in the **visual cortex**. When blocking excitatory postsynaptoc potentials, *tetanic stimulation of layer IV neurons* resulted in *iLTP of layer V neurons* postsynaptically mediated by increased *GABAA receptor currents*. Interestingly, the tetanic stimuli used were much like the stimuli used to evoked excitatory LTP (eLTP) in hippocampus as described above, and conditions favoring iLTP were much the same as the conditions needed to establish eLTP in the hippocampus (Komatsu, 1994).

**References**
**-** Kang *et al*., *Nature Neurosci* (1998); **1**(8):683-92
**-** Komatsu, *J Neurosci* (1994); **14**(11): 6489-99
**-** Rannals & Kapur, *J Neurosci* (2011); **31**(48): 17701–12
**-** Sieber *et al*., *J Neurosci* (2013); **33**(40): 15675-85

**Further Reading**
**-** How do neurons decide how to alter their output signals?
> 4 votes

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Tags: cognitive-neuroscience, plasticity
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# Question
Title: Are there "awareness" related mirror neurons or processes in the brain that get activated by awareness?
I'm reading the "The Power of Now" book by Ekhart Tolle, in which he describes a spiritual practice by which attention/awareness is focused on the currently experienced mental state. For example, anger, frustration or jealousy are observed without letting them take over. Tolle describes the outcome of this practice as something along the lines of "these emotions are transmuted into awareness". **I'm interested if there's any evidence in cognitive science to support his claim.**

The description reminds me of mirror neurons - observing an emotion in others "infects" the observer with the same emotion. There's a small number of deeply connected mirror neurons that permeate the human brain

This makes me ask the question - **are there "awareness" related mirror neurons or similar structures that get activated by one's own awareness?** By which process could the experience of observing emotion increase awareness of the observer?

Update: this wikipedia article has a very brief section on mirror neurons and self awareness:

> V.S. Ramachandran has speculated that mirror neurons **may provide the neurological basis of human self-awareness**.\[70\] In an essay written for the Edge Foundation in 2009 Ramachandran gave the following explanation of his theory: "... I also speculated that these neurons can not only help simulate other people's behavior but can be turned 'inward'—as it were—to create second-order representations or meta-representations of your own earlier brain processes. This could be the neural basis of introspection, and of the reciprocity of self awareness and other awareness.

# Answer
> 4 votes
Mirror neurons are actually quite a contentious area in cogsci. The debate is most certainly not settled as to what role they play, and whether they even exist, in humans. In short though, my argument would be that there are no *specific* awareness related mirror neurons in the brain because mirror neurons themselves *are* awareness. Again, this is an extremely contentious issue in cogsci, and there is no one answer widely accepted at the moment -- I'll just try to explain and justify my thoughts.

It's important in anything that's being discussed to have a working definition of the matter at hand. Personally, I would disagree with your definition of naming them "emotion infectors", instead opting to assume that mirror neurons are very specialised cells allowing for the reenactment of sensory-motor information (Rizzolatti et al.).

Gibson gave us a pretty neat applied example of this in the form of affordances. These are action possibilities possessed by items, but perceived by an agent (see Norman's review for a neat explanation as to why this changed) -- in short, a rock doesn't want us to throw it, but a human might want to throw a rock. Additionally, a mouse might see the same rock and, being unable to lift it and throw it, decide instead to hide behind it from predators. At the same time, a savvy cat may suss out what's actually going on... What does this mean for mirror neurons? Specifically that this network of cells allow us to understand actions, and create new ones, by parasitizing upon motoric and sensory systems. Essentially, *our experience of the world is bound by our bodily constraints*.

So what does this mean for our experience of abstract concepts? Domains like love, time, depression, and even awareness aren't physical entities, but metaphysical ones. These are conceptually understood (Lakoff). Time *flies*, we are *down in the dumps* when depressed and -- the most cheesy of all -- love *hurts*. Time doesn't actually fly, we don't shrink when we're depressed and love doesn't actually physically hurt, but we scaffold what is concrete (i.e. sensory-motor information) to the abstract in order to understand it (Veale & Keane).

So, **I don't believe that a mirror neuron network would exist for a process like awareness, because the mirror neuron network itself *is* awareness.** It's what provides us with a specific ability to understand the environment, to understand actions and, perhaps most importantly, understand ourselves.

# Answer
> 2 votes
With regard to emotions, it may be more useful to think about things in terms of interoception and attention. Interoception involves awareness of one's inner bodily sensations (e.g., pleasantness/unpleasantness, high/low arousal; Craig, 2002), and we can (rapidly) direct our attention to shifts in these sensations.

Changes in our inner physiological sensations are occurring constantly, but only when we foreground these changes in our attentional field (and make meaning of them) do we consciously experience an emotion (Barrett, 2014).

In general, interoception and attention as involved in emotion recruit the "salience network" (e.g., parts of the insula, parts of the cingulate cortex, etc.), which is involved in body-directed attention ("The Neuroscience of Construction," Oosterwijk, Touroutoglou, & Lindquist, 2014). We also make use of the frontoparietal network (e.g., dlPFC, mCC, etc.), involved in executive attention, which might mediate our ability to foreground mental states into awareness. In this sense, **it seems unlikely that mirror neurons alone are responsible for awareness of one's emotions; instead, broadly distributed neural networks might be involved.**

Paula Niedenthal has mentioned a potential role for mirror neurons in the simulation of sensorimotor experiences of emotions in the body. However, I don't think this corresponds to your hypothesis.

I'm otherwise not quite sure if I answered your question, but hopefully this clarifies something for you.

# Answer
> 1 votes
Here is an excellent article on self awareness and associated phenomena. The author (his quote is linked in the original question) describes various forms of brain damage and psychiatric conditions and their impact on (self)awareness and perception of the world. He mentions mirror neurons on multiple occasions.

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Tags: cognitive-psychology, emotion, cognitive-modeling, mirror-neurons, awareness
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# Question
Title: Is inhibitory brain circuitry involved in cross-modal sensory perception?
In many research articles, a vague description of a inhibitory circuitry in the brain is mentioned. This is presented as an inhibitory mechanism that prevents input from one sensory modality to excite another region (for example touch exciting visual cortex) or in general prevents any signal not coming from the visual nerve to excite the visual cortex. And that preventing test subjects from their sight (blindfolding for a longer period) interferes with those inhibitory circuits and deactivates them. The results are presented here where subjects started having hallucinations and perceiving things even though totally blindfolded. I am interested to know if there is some active research about those inhibitory circuits in the brain and if they are well understood.

I am trying to find out if normally sighted or normally hearing people could get visual/auditory information from both the original sense and through the skin via an electrotactile pattern through a sensory substitution device, to see if passive learning can be achieved.

# Answer
As far as I know, there is just one article that explicitly mentions the generation of cross-modal qualia, i.e., **visual qualia in response to tactile stimulation** (Ortiz *et al*., 2011). Before continuing about this article I do wish to emphasize it is a single, **isolated study** that hasn't been supported by other studies at the time of this writing. Moreover, the journal PlosONE is not my favorite and a bit of a strange journal to throw such an important observation in. I would have trusted this work more if published into a more appropriate journal for such strong claims, such as *J Neurosci*. Having said that:

The authors trained 18 blind subjects and 10 sighted, blindfolded controls for 3 months, on a daily basis using a tactile vision-substitution device; a vibrotactile display equipped with a camera. They deployed a grating acuity task and **7 out of 18 subjects reported 'seeing' visual qualia** after 3 months, i.e., these subjects started seeing the gratings instead of feeling them. It was **only blind folks** that reported this, not any of the sighted controls. Those blind folks reporting qualia showed **increased activation of the primary *visual* cortex** upon using the *tactile* device. The authors conclude that recruitment of the deafferented V1 in blind people led them to 'see' the tactile stimuli after sufficient training (Ortiz *et al*., 2011).

You are right that it is believed that a **disintegration of inhibitory circuits** in the cortex is believed to underlie crossmodal cortical recruitment of (e.g.) the visual cortex to tactile stimulation (Stronks *et al*., 2015). Chronic visual deprivation is believed to reduce the inhibitory circuits, while visual stimulation is believed to enhance them. For example, tetanic stimulation of inhibitory neurons (presumably through GABAA) resulted in more long-term potentiation of inhibitory responses in young rats than in adult rats (Komatsu, 1994). This is in line with the theory that **shaping of the brain is critically dependent on sensory input in early life**, i.e., inhibitory circuits are thought to be actively developed through experience, resulting in containment of visual processing in the visual cortices and tactile processing in the somatosensory cortex etc. Note, however, that even V1 has shown to be multimodal even in normally sighted folks, i.e., while V1 is dedicated to visual processing, it is not exclusively devoted to it. One theory about ***synesthesia*** is that the development of inhibitory circuits is compromised, leading to crossmodal activation in folks without any sensory disability. This theory has made people conclude that babies are all synesthetes (e.g., Wagner & Dobkins, 2009).

**References**
**-** Komatsu, *J Neurosci* (1994); **14**(11): 6489-99
**-** Ortiz *et al*., *PlosONE* (2011); **6**(8): e23264
**-** Stronks *et al*., *Brain Res* (2015); **1624**: 140–52)
**-** Wagner & Dobkins, *JOV* (2009); **9**: 699
> 4 votes

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Tags: perception, neurophysiology, sensory-perception
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# Question
Title: Are the human cerebral hemispheres only connected via the corpus callosum?
Are the human cerebral hemispheres only connected via the *corpus callosum*? Or is there any other structure for interaction between the left and right hemispheres?

# Answer
> 7 votes
The *corpus callosum* is a massive horizontal white matter tract (commissure) that connects the two hemispheres and it is considered the most important route of communication between the hemispheres.

However, there are five additional commissures that cross the midline, namely:

1. Anterior commissure, connecting the two olfactory bulbs and the temporal cortices;
2. Hippocampal commissure (psalterium), connecting the two hippocampal formations;
3. Habenular commissure, connecting the habenular nuclei;
4. Posterior commissure, connecting the pretectal nuclei, mediating the consensual pupillary light reflex;
5. Supraoptic commissures (a. Gudden's commissure, or ventral supraoptic decussation connecting the medial geniculate bodies and b. Meynert's commissure, connecting the two suprachiasmatic nuclei*).

Below figure shows the corpus callosum and the anterios commissure:

Saggital section through the human brain showing the *corpus callosum* and *anterior commissure*. Source: Brain Atlas.

\*The exact connection of Meynert's commissure I am unsure of. This is the best I could do.

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Tags: neuroscience, neuroanatomy
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# Question
Title: Personality trait in which the person's style is evident regardless of the situation?
What is the term for the personality trait in which a person's style is evident in all they do? The person's particular behavior patterns expresses the attitudes and inner characteristics of the person, regardless of the situation. A person with this trait puts a little bit (or a lot) of themselves in all they do. In contrast, other people may blend in more and adapt their behavior more strongly to what is expected by others.

I once read about this term in a personality model article online and have never seen it since.

# Answer
You may be referring to people who are low in **self-monitoring**.

Wikipedia has a good summary:

> Self-monitoring is defined as a personality trait that refers to an ability to regulate behavior to accommodate social situations. People who closely monitor themselves are categorized as **high self-monitors** and often behave in a manner that is highly responsive to social cues and their situational context. High self-monitors can be thought of as social pragmatists who project images in an attempt to impress others and receive positive feedback. Conversely, **low self-monitors** do not participate, to the same degree, in expressive control and do not share similar concern for situational appropriateness. Low self-monitors tend to exhibit expressive controls congruent with their own internal states; i.e. beliefs, attitudes, and dispositions regardless of social circumstance. Low self-monitors are often less observant of social context and consider expressing a self-presentation dissimilar from their internal states as a falsehood and undesirable. People who are unwilling to self-monitor and adjust their behavior accordingly are often aggressive, uncompromising, and insistent with others. This may make them more prone to condemnation, rejection, and the possible consequent feelings of anger, anxiety, guilt, low self-concept, isolation, and depression. Even the occasional indiscretion can make social situations very awkward, and could result in the loss of a friend, co-worker, client, or even job. Those who are willing to adjust their behavior will often find that others are more receptive, pleasant, and benevolent towards them.

Self-monitoring is usually measured with Snyder's (1974) Self-Monitoring Scale or variants thereof.

The scale measures agreement to items such as:

> I find it hard to imitate the behavior of other people.
>
> My behavior is usually an expression of my true inner feelings, attitudes, and beliefs.
>
> At parties and social gatherings, I do not attempt to do or say things that others will like.
>
> I can only argue for ideas which I already believe.

**References**

Snyder, M. (1974). Self-monitoring of expressive behavior. Journal of personality and social psychology, 30(4), 526.
> 2 votes

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Tags: personality
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# Question
Title: Are introverts more talkative in written form than extroverts?
We all know that extroverts are in general more talkative than introverts in oral form. But how about written communication?

After having talked with lots of people on the internet and met several of them, I have the impression that the most talkative online are the most introverted offline and vice versa.

---

Half a year after posting this question I've got a personal confirmation from one extrovert I talked to: He told me doesn't like to write much, because he prefers the more 'personal' communication from spoken communication. Another extrovert told me he prefers speaking on the phone rather than writing messages. Introverts, on the other hand, often dislike phones and prefer messages.

**So there does indeed seem to be something in my theory, but I need more objective, statistical datas on it.**

# Answer
> 4 votes
**1. Are extraverts more talkative than introverts in oral communication?**

Yes they are. The (probably) best evidence can be found in research by Mehl et al. (2006) who "tracked 96 participants over 2 days using the Electronically Activated Recorder (EAR), which samples snippets of ambient sounds in participants’ immediate environments". The correlation of extraversion with word count was .29, indicating that extraversion was related to more talkativeness.

**2. Are introverts more talkative in written communication?**

It does not seem so. A study that addresses your question has been done by Gill and Oberlander (2002). They asked participants to compose two emails to a good friend. The more extraverted they were, the longer were the emails (beta = .20). Thus, this study was not in line with your intuition that introverts are more talkative in written form. Of course, you may argue that under some circumstances (maybe when writing a diary or a book) your hypothesis may still hold. However, judging from this study, if it exists at all, this does not seem to be a general effect.

There are some differences in writing style and content, however. For example, introverts seem to use a more concrete and focused language (Gill & Oberlander, 2002). Furthermore, introverts tend to use longer words (Mehl et al., 2006) which may be in line with Alex Stone's comment.

**References**

Gill, A., & Oberlander, J. (2002, August). Taking care of the linguistic features of extraversion. In Proceedings of the 24th Annual Conference of the Cognitive Science Society. Fairfax, VA.

Mehl, M. R., Gosling, S. D., & Pennebaker, J. W. (2006). Personality in its natural habitat: Manifestations and implicit folk theories of personality in daily life. Journal of Personality and Social Psychology, 90(5), 862–877. http://doi.org/10.1037/0022-3514.90.5.862

# Answer
> 0 votes
I found a study that says introverts and extroverts are about equally talkative in written form:

> "There is little empirical information about differences in computer-mediated communication related to personality. However, it has been widely speculated that introvertive personality traits are especially appropriate for CMC. The results of the present study are consistent with these predictions. Introverted participants sent as many messages as did extraverted participants, and their messages contained more information. As regards gender, males sent longer messages than did females, but their messages did not contain more information."

This study also supports that introverts are more precise in their communication (Gill & Oberlander, 2002).

One might say that introverts are less interested in talking for the sake of it, but they may communicate larger amounts of information. This would further imply that communication, for an extrovert, is more about the social interaction and not as much about giving information.

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Tags: social-psychology, communication, introversion, extraversion, preferences
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# Question
Title: How does one respond to an ADD/ADHD diagnosis of one's self or one's child?
I read:

> Is ADHD even a thing?
>
> This kind of question can be offensive to some. The same kind of thing can be applied to other conditions:
>
> Is depression even a thing? Or are they just lazy? Is gender disphoria even a thing? Or have they just sexually confused? Is homosexuality even a thing? Or are they just a deviant? Is otherkin even a thing? Or are the just a teenager looking for a unique identity?

Apparently, there is much controversy over ADHD, according to Wiki (not enough reputation)

Part 1:

What is a diagnosed person to do? How does one evaluate methods used by a doctor? How does one evaluate if prescribed medicine and dosage is right or at least not severely wrong?

I'm guessing initial prescription, if any, is going to be experimental. From there we see if dosage needs to increase or decrease or if medicine needs to be changed or stopped. How then should one evaluate a doctor's decision?

Part 2:

Why not controversy over depression? Bipolar? Schizophrenia?

Some psychologists seem to believe ADD/ADHD is a myth. Is there any truth to such?

The blog also points out how homosexuality was wrongly considered a disorder. How do we know ADD/ADHD won't turn out like that?

# Answer
There actually is the same kind of controversy over depression. The French documentary *Dépression, une épidémie mondiale* nicely summarizes how a well-meant change in diagnostic criteria (from DSM-IV to DSM-5) backfired and the pharmacoceutical industry now use this to diagnose every sadness or exhaustion as depression with the intention to sell drugs and make money.

There has also been controversy over schizophrenia for at least two hundred years. Other mental disorders are equally highly controversial. It is just that ADHD is a "fashion disorder" today and therefore covered by the media, which gives laypeople the impression that only this disorder is controversial.

As for ADHD, we live in a society that favours certain personality traits and disfavours others, and those kids that don't sit still very well, need a higher input speed, or are simply socially maladjusted, are often diagnosed with ADHD, although they are perfectly healthy and normal and would only need a different kind of learning environment or better familial support.

On the other hand, this does not mean that ADHD does not exist. If the diagnosis was given by an expert after careful investigation, then the patient will certainly profit from therapy. But the therapy cannot be deduced from the diagnosis alone. It must take into consideration the etiology (what caused the disorder?) and the circumstances (how does the patient live?), as well as the personality of the patient. Because the same symptoms of the same disorder can have widely varying causes, and you want your therapy to address those causes and not just ease the symptoms.

Therefore a meaningful diagnosis will include an analysis of the cause. ADHD can be genetic, caused by harmful substances, or psycho-social. Therapy will differ in each case.

If you want to evaluate a diagnosis and recommended therapy, I would recommend you go see another expert. Evaluating them yourself would require you study medicine and psychology to an extent probably not feasible. Be extremely careful of reading stuff on the net! Much of what you find there is published by companies who are in search of patients to sell medication to, or by laypeople.

I don't know where you live, and probably don't know how you can find trusted experts in your country. In Germany, where I live, the best path to take would be to approach therapeutic organizations or even your health insurance and ask them for whom you should turn to.

Generally, psychiatrists appear to be more likely to prescribe medication, while psychologists seem to prefer non-medical therapy. The best therapy for many mental disorders is a combination of both, with medication used to alleviate the current symptoms, and psychotherapy working mid- to long-term on changing behavior (and personality) so that medication is no longer necessary or can at least be reduced. I know people with ADHD who live well without medication, simply by creating for themselves the environment that they can flourish in.

All the best.

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# tl;dr

Find a doctor you can trust, and trust them.
> 3 votes

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Tags: measurement, abnormal-psychology, methodology, psychiatry, adhd
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# Question
Title: Why did humans develop the "sense of humour"?
Speaking from the point of view of evolutionary psychology, is there any research that demonstrates why a 'sense of humor' may be a part of our mental mechanisms?

Does research show that it is a way to quickly decrease stress levels?

# Answer
Interestingly, the same question you asked has been asked since quite some time:

***The Act of Creation*, 1964 - Arthur Koestler**

> What is the survival value of the involuntary, simultaneous contraction of fifteen facial muscles associated with certain noises which are often irrepressible? Laughter is a reflex, but unique in that it serves no apparent biological purpose; one might call it a luxury reflex. Its only utilitarian function, as far as one can see, is to provide temporary relief from utilitarian pressures. On the evolutionary level where laughter arises, an element of frivolity seems to creep into a humorless universe governed by the laws of thermodynamics and the survival of the fittest.

Firstly, like all other narratives built by evolutionary psychologists, it is difficult to back up speculations with empirical evidence. Since we are going back far back into the evolutionary history of *homo sapiens*, we will be dealing with what I would call "well-informed speculation".

**Quoted from *The Mating Mind* (2001) by Geoffrey Miller.**

> To traditional evolutionary psychologists, human abilities like music, humor, and creativity do not look like adaptations because they look too variable, too heritable, too wasteful, and not very modular. But these are precisely the features we should expect of fitness indicators. If a human mental trait shows large individual differences, high heritability, high condition-dependence, high costs, and high correlations with other mental and physical abilities, then it may have evolved through sexual selection as a fitness indicator. (pg. 132-133)

**Sexual Selection**

Notice that he also mentioned your speculation about decreased stress levels:

> Some theories of humor have proposed that laughter evolved to promote group bonding, discharge nervous tension, or keep us healthy. The more laughter the better. Such theories predict that we should laugh at any joke, however stupid, however many times we have heard it before, yet we do not. A good sense of humor means a discriminating sense of humor, not a hyena-like shriek at every repetitive pratfall. Such discrimination is easy to understand if our sense of humor evolved in the service of sexual choice, to assess the joke-telling ability of others.

Furthermore, I recommend that you read this review of Robert Mankoff of “Inside Jokes”: The Hidden Side of Humor. (2011) and of course the book itself. It sheds a strong light onto your question.

---

**Sources:**

Matthew M. Hurley, Daniel C. Dennett, and Reginald B. Adams Jr., *Inside Jokes: Using Humor to Reverse-Engineer the Mind*. MIT Press, 2011, 376 pp., ISBN-13: 978-0262015820

Koestler, Arthur. 1964. *The Act of Creation*, Penguin Books, New York

Miller, G. (2000), *The Mating Mind: How Sexual Choice Shaped the Evolution of Human Nature*, London: Heineman, ISBN 0-434-00741-2 (also Doubleday; ISBN 0-385-49516-1)
> 4 votes

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Tags: evolution, humour, evolutionary-psychology
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# Question
Title: What are the consequences of prolonged cognitive dissonance?
We know that situations that induce cognitive dissonance cause a variety of interesting behaviors in humans.

But do we know why relieving cognitive dissonance is such a powerful motivator? What happens if that dissonance is not relieved?

Are there any known cases from history or animal experiments where humans or animals were subjected to prolonged cognitive dissonance? If so, what happened in those cases?

# Answer
**Summary** (copied from last paragraph)

It appears that extended exposure to cognitive dissonance ignites an initial emotional reaction that is then mediated by the rationalization process. If no rationalization can be made, or if the emotion cannot be effectively controlled by the individual, then **the initial emotional reaction may grow more powerful, resulting in mood-regulation disorders such as depression, anxiety, or post-traumatic stress disorder.** \[5\]

**Details**

Cognitive dissonance is thought to reveal a human's internal desire for consistency. Those who experience cognitive dissonance become psychologically uncomfortable, and thus may take measure to reduce situations that may induce cognitive dissonance. \[1\]

Humans have a tendency to want to explain how the world works. There is a discomfort in not 'knowing'. In cognitive dissonance theory, there are several underlying themes, most notably that of religion in cognitive dissonance. Insofar as the theory goes, religion is one helpful mechanism for avoiding cognitive dissonance, as religion often provides an explanation for the nature and generation of the world, as well as a set of guidelines to follow. This provides humans with internal consistency. Skepticism/loyalty to the 'objective' nature of the scientific method can be another form of avoiding cognitive dissonance. \[2\] Rejection of any sort of method of navigation (or purpose) in the world often lends itself to a feeling of nihilism, though this is not always related to cognitive dissonance as it is defined.

Sigmund Freud himself observed several instances of what he coined as "Das Unheimliche" -- German for 'the opposite of what is familiar', and translated into English as 'the uncanny'. He describes it as the experience of that which is strangely familiar, not just mysterious. Though the term is not an adequate synonym for 'cognitive dissonance', it is nonetheless relevant in the reaction it produces:

> Because the uncanny is familiar, yet incongruous, it has been seen as creating cognitive dissonance within the experiencing subject, due to the paradoxical nature of being simultaneously attracted to yet repulsed by an object. This cognitive dissonance often leads to an outright rejection of the object, as one would rather reject than rationalize, as in the uncanny valley effect.

This initial emotional response is supported by neuroscientific literature when we consider cognitive dissonance as an observable phenomenon. College students who were told to write an argumentative essay in support of a stance that they did not agree with showed increased activity in the anterior cingulate cortex. Next, the left frontal cortex was activated, which is known to activate the 'approach motivational system'. \[3\] The motivational directions model asserts that this system regulates one's response to their own anger. If the situation cannot be controlled or changed by the person, they may have less motivation to reduce or regulate their anger, and other emotions may arise. \[4\]

Thus, it appears that **extended exposure to cognitive dissonance ignites an initial emotional reaction that is then mediated by the rationalization process. If no rationalization can be made, or if the emotion cannot be effectively controlled by the individual, then the initial emotional reaction may grow more powerful, resulting in mood-regulation disorders such as depression, anxiety, or post-traumatic stress disorder.** \[5\]

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Sources:

\[1\] Festinger, L. (1957). A Theory of Cognitive Dissonance. California: Stanford University Press.

\[2\] R. A. Wicklund, J. W. Brehm. (1976). Perspectives on Cognitive Dissonance.

\[3\] Beauvois, J. L., Joule, R. V., 1996. A radical dissonance theory. London: Taylor and Francis.

\[4\] Harmon-Jones, E., Mills, J., Cognitive Dissonance: Perspectives on a Pivotal Theory in Social Psychology. American Psychological Association, Washington, DC, pp. 71–99.

\[5\] Hull, A.M. (2002). Neuroimaging findings in post-traumatic stress disorder. The British Journal of Psychiatry 181: 102-10.
> 4 votes

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Tags: cognitive-psychology, social-psychology, cognitive-dissonance
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# Question
Title: Parasite that takes over cognitive functions
I am testing an idea for a book. The backbone of the story is that there exists a parasite that can enter the brain of a creature and take over its cognitive functions. I imagine that it could wire itself in some central part of the brain or neural system, but I am not an educated physician. Let us assume that the being infested is a human. I would like some input:

1) Is this at all possible? I know it is possible with parasites that infest insects.

2) What area of the brain/neural system would it have to take over, or how at all could this happen?

3) The parasite just hijacks the brain, does not destroy it. If it decided to retreat, how much of the information/memories acquired during the infestation period could it carry with it? How much of the events happened during this period would be accessible to the subject after retreat?

4) If we assume a parasite that itself has some cognitive ability, and does not act just out of infestation instinct, how large would it have to be in order to be able to have its own (even basic) thoughts, and retain memories of the subject?

I would appreciate any input on these questions, and any related thoughts you might have.

This question has been put on hold because *answers to this question will tend to be almost entirely based on opinions, rather than facts, references, or specific expertise*. With all due respect to the hard work of the moderators, I have to disagree. To begin with, all answers to all questions and even the questions themselves are exclusively opinion-based. Otherwise we would have to assume that there really is any truth that can be objectively be known and agreed upon. No one has ever been able to prove that anything besides our consciousness exits. But if even we have to tone down our agnostic perspective (why do we have to do that?) if you mean that there is not (in the world that you believe you perceive) enough evidence and research to support informed answers, then again this is not right. A user replied with an example of something like this occurring (evidence) and another with a very elaborate answer with examples and cited references to how something like this could happen. I strongly believe that more informed answers can come through.

# Answer
> 2 votes
I can't give you an informed response to questions 1 and 2 though I do know that parasitic wasps inject toxin into a spider, lay an egg on the back of the spider and cause it to spin a web that will protect the egg. So some form of behavioural control of spiders is possible. Spider brains are much simpler than human brains but there was a paper by Strausfeld and Herth in *Science* April 2013 that argued that there are "deep similarities in how the brain regulates behavior" in both insects and humans. There are similarities of function and structure between the 'central complex' of insects and the basal ganglia of humans. So I am guessing your parasite would need to target the basal ganglia.

However, the idea that the parasite might acquire memories and information is a totally different scenario and extremely unlikely. Memory is a complex phenomenon but it appears to be largely based on the re-activation of particular neuronal pathways. Most memory is largely inactive most of the time, it has to be re-created each time (and hence is inherently slightly different each time). I suggest the meaning of such activation patterns is intrinsically linked to a) the other neural activation patterns occurring in the brain at the same time and b) the human body and its experiences. In any case, for a parasite to 'capture' memories it would need to be able to emulate those neuronal pathways; and even if it did, it would probably 'mean' something entirely different. Even if it could 'copy' memories, it would not somehow take the memories away from someone. Memories can be destroyed, or made inaccessible but only by disrupting the activation patterns (destroying neurons, blocking or destroying triggering mechanisms etc.).

You also should be aware that even when neuronal pathways are activated,it does not mean that we are aware of them. In fact we are unaware of most activated 'memory' (see Kahneman 2011). There is a difference between implicit memory (and automatic behaviors) and explicit memory. Part of the brain, the left ventrolateral prefrontal cortex, is activated when we are consciously thinking or ruminating about something, solving difficult problems, etc. It appears to tap into memories and make them explicit so we can think about them or use them for computations etc. As an aside, the LVLPFC is a long way anatomically from the basal ganglia.

Another important distinction for your thesis is the difference between procedural memory (memory of motor and cognitive skills etc.) that, for example, allows one to type without looking at the keys: and declarative memory or memory about things. The parasite I mentioned earlier presumably is able to trigger some part of procedural memory: but it seems highly unlikely that it might also trigger declarative memory, or even access declarative memory, which largely occurs in a different part of the brain. However, declarative memory is severely affected by damage to the hippocampus so it is perfectly possible that a parasite might be able to induce amnesia. However, if my very weak memory serves me, the hippocampus is not adjacent to the basal ganglia so it is unlikely that the same parasite could control behaviours and take memories.

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Tags: neuroscience, memory, cognitive-neuroscience, consciousness, neurophysiology
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# Question
Title: How is doing a manipulation check different from doing the analysis on the main dependent variable?
How is doing a so-called manipulation check (i.e. checking to see whether the different groups actually differ for different levels of the independent variable) different from doing - as a main analysis - e.g., an ANOVA to see if the independent variable has had an effect on the dependent variable? From reading papers, it seems people just do manipulation checks *prior to* the main analyses.

# Answer
It depends on what you mean by manipulation check.

**Manipulation check to filter participants:** A manipulation check is usually done to verify that some experimental manipulation has had some preliminary effect. For example, in one of my studies I asked people to answer a personality test (a) honestly, (b) as an ideal worker, and (c) as the worst possible worker. I asked each participant how they intended to answer the personality test. The **manipulation check** was there to verify that they had understood the instructions. In this case, the manipulation check was used to potentially exclude participants who failed to pass the manipulation check.

**Manipulation check to verify group-level effect:** Of course, you could perform such manipulation checks on an entire group using group comparison tools such as ANOVA for a numeric variable or chi-square for a categorical outcome. For example, in some psychological studies, the experimenter may attempt to manipulate mood as baseline manipulation. Thus, they may want to get check whether the group that has been made to experience negative affect does on average experience more negative affect. In that case an ANOVA makes sense.

**Checking approximate group equivalence::** A third case is where you are merely checking whether the groups are the same at baseline and that has more to do with how participants were allocated to groups. It doesn't sound like you are talking about this case.

**Using manipulation check outcome as covariate:** In general, manipulation checks are typically reported prior to conducting main analyses. In this sense, they are a bit like assumption tests. They verify that some experimental manipulation has worked and that you can now proceed to examine the effects of substantive interest. That said, you could do a range of other analyses where the outcome measure in the manipulation check is included in your analysis of the substantive outcome. For example, if you were studying task performance in two groups, one with a positive mood induction and one with a negative mood induction, you could run an ANCOVA where condition was your independent variable, measured mood (i.e., the manipulation check variable) was your covariate, and task performance was your dependent variable.
> 3 votes

# Answer
Primarily, a manipulation check is an indicator of the **internal validity** of an experiment.

If the manipulation of your independent variable makes a statistically significant difference on the dependent variable, you have evidence for a causal effect of the manipulation. The manipulation check can give you more certainty that this effect is due to changes in the construct you are interested in.

For example, imagine you manipulated mood by showing a happy versus a sad movie clip. Subsequently, this affects the extent to which people are persuaded by weak versus strong arguments (argument strength doesn't matter in the happy movie condition). Showing that your manipulation has affected mood in the intended way with a manipulation check (better mood in the happy than in the sad movie) allows you to be more certain that this has something to do with mood. If your manipulation check would not show a mood difference, the difference on the dependent variable might be caused by some other aspect of the manipulation (for example differences in arousal).

The manipulation check also allows to do **correlational analyses** to strengthen this conclusion: Are changes in the dependent variable mediated by changes in the manipulation check? (Does persuasion change to the extent that mood has been altered?)

More pragmatically, if you have no effect on the dependent variable, the manipulation check may give you some insight. Is it because the manipulation failed? (No/to small effect on the manipulation check?) Or is it because is the problem on the side of the dependent variable? (Your measure doesn't work or, heaven forbid, your hypothesis is wrong).
> 3 votes

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Tags: methodology, experimental-psychology, validation
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title: Why do we like stories?

text:
# Question
Title: Why do we like stories?
Almost everyone likes a good story, the way in which it is delivered matters, but most people love a good story in one form or another, whether it's delivered through conversation, a book, a video game, a movie, or even if it's just them trying to make sense of how a shoe got into a swimming pool (That's right, it's ok if the story is created in your own mind, it's still a story, so we seem to like telling stories as much if not more than we like hearing or reading them).

So why do we like stories at all? Why do some of us like stories to the point of obsessing over them?

How does this happen? And is this something that can be controlled (i.e. could you make someone who prefers violent stories prefer switch over to preferring romance stories? Can someone be conditioned to not be interested in any stories at all no matter what they may be about?)

Why is it also that once we start with a story, it can be hard to stop because you want to know what happens next or want to know how it ends? Why do some of us care if people "spoil" the ending for us by telling us what happens before we see or read or hear it, while some of us seem not to care?

Has any real research been done on this?

# Answer
> 3 votes
I'll try to roughly answer your question. It's not an easy one, and by no means does it have a narrow answer. Scientists have suggested, like you mentioned that stories show a lot about the basis of human thought

**So why do we like stories at all?**

From "The Storytelling Animal" (Jonathan Gottschall)

> “Some thinkers, following Darwin, argue that the evolutionary source of story is sexual selection, not natural selection. Maybe stories, and other art forms, aren’t just *obsessed with sex*; maybe they are ways of *getting sex* by making gaudy, peacocklike displays of our skill, intelligence, and creativity—the quality of our minds. Thumb back a few pages to that image of the Kung San storyteller on page 19. Look at the young woman sitting to the storyteller’s left—very pretty, very rapt. That’s the idea.
>
> Or maybe stories are a form of cognitive play. For the evolutionary literary scholar Brian Boyd, “a work of art acts like a playground for the mind.” Boyd suggests that the free play of art, in all its forms, does the same sort of work for our mental muscles that rough-and-tumble play does for our physical muscles.
>
> Or maybe stories are low-cost sources of information and vicarious experience; maybe, to modify Horace, stories delight *in order* to instruct. Through stories we learn about human culture and psychology, without the potentially staggering costs of having to gain this experience firsthand.
>
> Or maybe story is a form of social glue that brings people together around common values. The novelist John Hardner expresses this idea nicely: "Real art creates myths a society can live by instead of die by." Go back again to the Kung San storyteller. Look how he has brought his people together skin against skin, mind against mind.

**Why do some of us like stories to the point of obsessing over them?**

> “Fiction, like cocaine, is a drug. People may invent high-minded aesthetic (or evolutionary) justifications for their fiction habits, but story is just a drug we use to escape from the boredom and brutality of real life. Why do we go to see a Shakespeare play, or watch a film, or read a novel? Ultimately, from Kessel’s point of view, it is not to expand our minds, explore the human condition, or do anything else so noble. We do it for kicks.
>
> Many evolutionary thinkers would agree with Kessel’s position. What are stories for? Nothing. The brain is not designed for story; there are glitches in its design that make it vulnerable to story. Stories, in all their variety and splendor, are just lucky accidents of the mind’s jury-rigged construction. Story may educate us, deepen us, and give us joy. Story may be one of the “things that makes it most worthwhile to be human. But that doesn’t mean story has a biological purpose. Storytelling, in this view, is nothing like the opposable thumb—a structure that helped our ancestors survive and reproduce. In this view, story is more akin to the lines on your palm. No matter what your fortuneteller claims, the lines are not maps of your future. They are side effects of the flexion of the hand.”

**How does this happen? And is this something that can be controlled?**

I couldn't find any experiment that, like you mentioned, discussed whether you can *change* someone's preference of what kind of stories they like. If someone finds any study, please mention it in the comments!

**Why is it also that once we start with a story, it can be hard to stop because you want to know what happens next or want to know how it ends? Why do some of us care if people "spoil" the ending for us by telling us what happens before we see or read or hear it, while some of us seem not to care?**

From this source, an excellent article on storytelling.

> Suspense works just as well as you’d expect
>
> The “cliffhanger” just may be the oldest trick in the writing book, especially writing for television, but there is a reason why it’s used so often…
>
> It works!
>
> Despite our numerous exposure to this method, our brain just can’t “get over” suspenseful moments: it’s a relationship that just won’t die, we will always want to know what happens next.
>
> In fact, suspense works so well that the hotly debated Zeigarnik Effect would have you believe that it’s the best way to kill procrastination.
>
> Research in that area seems to point to humans being much more inclined to finish something that has already been started (researchers interrupted people doing “brain buster” tasks before they could complete them… nearly 90% of people went on to finish the task anyway, despite being told they could stop).
>
> Suspense in stories really allows you to create an addictive narrative, as long as the suspense appears early enough to capture interest, and doesn’t keep people hanging on forever

**Has any real research been done on this?**

I might elaborate on this further. I don't want to comment without first exploring the research I have quoted to see whether they are good studies. If anyone else knows of any experiments related to this field, please mention it in the comments.

Co-creating stories: Collaborative experiments in storytelling Management Learning November 2010 41: 507-523, first published on June 28, 2010

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**Sources:**

*The Storytelling Animal: How Stories Make Us Human* by Jonathan Gottschall (ISBN-13: 978-0547391403 ISBN-10: 0547391404)

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Tags: addiction, evolutionary-psychology
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# Question
Title: Can someone clarify whether the term "heuristic" as used in psychology can be used to refer to an intentionally chosen strategy?
In my cognitive psychology class, we discussed heuristics. An example of a heuristic is loss aversion. Thus, in this context, a heuristic seems to be a general rule of thumb for how people *behave*.

But I was under the impression a heuristic was "any approach to problem solving, learning, or discovery that employs a practical methodology not guaranteed to be optimal or perfect, but sufficient for the immediate goals" (source: Wikipedia).

As an example, let us consider a coat rack. One might suppose that putting my coat on a coat rack is a type of problem solving strategy because it allows me to always find my coat at that location. Thus, the problem being solved would be "How can I always know where my coat is."

Can someone clarify whether the term "heuristic" as used in psychology can be used to refer to an intentionally chosen strategy (as opposed to loss aversion which is just "instinctive")?

# Answer
**Short Answer:**

Yes it can.

**Long Answer:**

According to Wikipedia,

> A *heuristic* is “any approach to problem solving, learning, or discovery that employs a practical methodology not guaranteed to be optimal or perfect, but sufficient for the immediate goals.” Source: https://en.wikipedia.org/wiki/Heuristic.

This is a good general definition that seems to adequately capture the meaning behind "heuristic" as used in different fields. However, one must be careful to understand the specific use in a given context.

With regard to psychology, there seems to be some confusion because there are both intentional and unintentional heuristics. Examples of unintentional ones are the availability heuristic. Some of the unintentional ones are more prominent and have received more attention and, as a result, I am not sure this distinction that there are "intentional" heuristics is always made.

However, according to Tversky and Kahneman (Nobel laureate in Economics),

> The term *judgmental heuristic* refers to a strategy ― whether deliberate or not ― that relies on a natural assessment to produce estimation or a prediction. One of the manifestations of a heuristic is the relative neglect of other considerations (Tversky and Kahneman, 294).
>
> Source: "Extensional Versus Intuitive Reasoning: The Conjunction Fallacy in Probability Judgment" by Tversky and Kahneman in *Psychological Review* Vol. 90 No. 4, 1983.

Note: the notion of a "judgmental heuristic" means simply a heuristic used in the mental faculty of "judgement," which I will not attempt to define.
> 2 votes

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Tags: cognitive-psychology
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# Question
Title: Do users of pictographically represented languages users have the same rates of dyslexia and dysgraphia?
I was wondering, given that a number represents a concept, unlike a letter that represents sound (that changes with context) - Do **pictographic language users have similar rates of *dyslexia* and *dysgraphia***?

# Answer
**Short answer**: Perhaps, but it is difficult to measure because the functional accounts of dyslexia and dysgraphia differ between alphabetic and non-alphabetic languages.

**Longer answer**: It has been argued that oral reading in Chinese can proceed via (at least) two pathways: the lexical semantic pathway (which supports reading for meaning), and the nonsemantic pathway (which connects representations of strokes, radicals, and characters to their phonological representations). \[1\]\[2\]

From Yin et. al. \[2\]:

> "...The patterns of acquired dyslexia and dysgraphia observed in Chinese cannot be identical to the patterns observed in alphabetic languages. This is because certain properties of the Chinese script do not allow direct comparisons between the disorders. For example, nonlexical stimuli in alphabetic scripts...cannot be constructed in Chinese. Thus, it will not be possible to replicate the pattern of preserved nonword processing in surface dyslexia and dysgraphia observed in English and Spanish."

The article stresses that the patterns of dyslexia and dysgraphia in Chinese are determined by the language 'environment', or the spatial characteristics of the script, and not the language itself. Since the language is spatial in nature, it is hypothesized that speakers use orthographic information from the character in order to determine the character's meaning. This means that if access to the semantics of a word is partially damaged, then surface level dyslexia can be observed in Chinese -- though, again, since the nature of the languages is different, it is not an exact 'replica' of lexographic dyslexia in alphabetic languages.

Thus, it is more common in non-alphabet languages for dyslexia and dysgraphia to be associated with oral or phonological deficits. Some studies have shown that Chinese may demonstrate 'tonal dyslexia' by providing the wrong tonal stress on a syllable, or by providing the wrong monosyllable for the word.

> "One view of phonological representations of Chinese words is that they have a non-linear structure containing separate syllabic, segmental (onset and rime) and supra-segmental layers...Tonal reading and writing errors result from impairment to the tonal tier or association between tonal and segmental tiers which leads to a dissociation between segmental and suprasegmental units, thus revealing the structure of the phonological lexicon."

Overall, given that there is no "universal" model of reading and writing, there is evidence that these dysfunctions in language processing arise *within* languages, not in spite of them, and thus take on different characteristics within each language. \[3\]

For individual characteristics among other non-alphabetic languages, feel free to look at the source material below.

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Source used: Acquired Dyslexia and Dysgraphia Across Scripts

\[1\] To understand this within the context of alphetic languages, the dual-route theory of reading aloud describes observable potential deficits in lexical understanding and in phonological understanding when reading words aloud.

\[2\] W. Yin et al. / Acquired dyslexia and dysgraphia in Chinese (p. 163-165)

\[3\] B.S. Weekes / Acquired disorders of reading and writing: Cross-script comparisons (p. 53)
> 2 votes

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Tags: cognitive-psychology, perception
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