(Why) Do US studies of violence and mental illness tend to report no link but European studies seem to find one? Studying the link between mental illness and violence seems a sure way to

get attention from the mass media, and
contradict some other study, and not necessarily one published that long ago.

A pretty old review (and not in some high impact venue) by Stuart (2003) seems to me to still hold water 15 years later with respect to a few general observations:

Definitive statements are difficult to make and it is equally possible to find recent literature supporting the conclusions that the mentally ill are no more violent, they are as violent, or they are more violent than their nonmentally ill counterparts. [...]
Because of the significant methodological challenges faced by researchers in this field, the nature of this association remains unclear. For example, violence has been difficult to measure directly, so that researchers have often relied on official documentation or uncorroborated selfreports. The prevalence of violence has been demonstrated to differ dramatically depending on the source. [...]

And it goes on to talk about confounders as the perennial problem of epidemiological studies.
Stuart also highlights a (highly cited) US-sample study of the "no-link" variety (at least if substance-abuse is controlled for), Steadman et al. 1998 ... and I certainly found some newer ones myself, Elbogen & Johnson (2009) or Anderson et al. 2012, just to mention some picked up by the press.
On the other hand, the Oxford group of Fazel has been publishing study after study on European samples including on Sweden (2015)
or UK, Finland and Netherlands (2017) that do find a link between depression and violence... and these have also been picked up the press. There are older studies in Scandinavian countries which concur; Hodgins et al. (1996) for instance.
So is this a trend? And (the really tough question) is there a meta-analysis of such studies that does moderator analysis (e.g. by meta-regression) to determine which study parameters matter most with respect to the finding? Is it the case that the Europeans are less violent overall so that the "inherent" violence of the mentally ill "stands out" in Europe but "gets lost in the noise" of the higher society violence in the US? (It certainly is the case the US is more violent than Sweden.) Or is it some other factor that is dominant, e.g. is depression more conductive to violence than other forms of severe mental illness (makes sense to ask since 2 of 3 US studies I've looked at aggregate severe mental illnesses — SMIs). To give you an example of the kind of meta-analysis I'm hoping to find, for ADHD prevalence it seemed that there might be geographical differences between US and Europe, but they turned out to be methodological.

I found a paper by Van Dorn et al. (2012) reanalyzing the same data as Elbogen & Johnson, and coming to a European-style conclusion of a link between SMI and violence. The difference in methodology came down (in this case) to:

important is spatio-temporal contiguity (i.e., the causal factor must be
spatially near the effect).

So merely lifetime SMI prevalence wasn't a good predictor but recent symptoms (within 12 months) were. That and the fact that the control group of Elbogen & Johnson apparently was not clean enough (of substance abusers) apparently tipped the scales.
But Eblogen didn't quote concede the field, and in a 2016 study on the exact same data (using 12 months window this time) but with more attention to confounders... found again in favor of their original findings:

Mediation analyses informed by the I3
model revealed
that the positive association between SMI and violence
was by and large indirect. Statistically controlling for
impellance and disinhibition completely wiped out any
positive relationship between SMI and violence.

This is somewhat similar result to what Anderson et al. (2012) obtained on different data after controlling for impulsivity and "present orientation" (using just two simple questions for these two factors!)

I have been away from here for a while as I have been concentrating on my University studies, however, I have just come back and boy have I come back at an opportune moment.  Your question showed a lot of research whilst being put together and this is an interesting topic of discussion as I have been discussing the subject of mental illness and violence myself with a couple of friends.

As you pointed out, Heather Stuart stated that

  Definitive statements are difficult to make and it is equally possible to find recent literature supporting the conclusions that the mentally ill are no more violent, they are as violent, or they are more violent than their nonmentally ill counterparts.

From what I have seen, I would agree with you that this still stands today as a response to your question.  The thing is, I have not seen an article which gives a definitive answer.

It is interesting to read the 2017 study on the FBC, RADAR and ALSPAC datasets you provided.  The thing to note with this study is that although

  In the additional sensitivity analyses, we also adjusted for other factors including parental criminality, conduct disorder, and maltreatment where data were available.

what about information regarding maltreatment etc. which was not available?  Those children who were subjected to undocumented external factors, which could affect their behaviours, would have been excluded from the adjustments and therefore, the statistics presented may be inaccurate.

Another point to make is that as the datasets seem to be based on self disclosures of violence, this, along with other issues raises all sorts of questions.

I would ask how the relevant studies defined violence when asking for the disclosures.  How were the questions put forward?  What was included in their definition of violence?  Was verbal and/or mental abuse considered to be violence or was the scope restricted to just physical violence?

This could be one reason why there is a discrepancy between US studies and European studies.  Another possibility is, were there cultural differences in play?

The differences in all the studies you pointed out using the Elbogen & Johnson data highlights the complexity of such a study.  What mental illnesses were covered in the studies?  Were any of the mental illnesses a result of (or made worse by) substance abuse, and if so, what is the prevalence of this factor?

There could also be all sorts of problems with interpretation of the data.  @ArnonWeinberg shows an example of possible misinterpretation of data when referencing Sweden as the rape capital of the world.  (See here for what I am — and possibly also what Arnon is — referring to).

There are so many questions which seem hard to answer with what I have seen and these sort of questions may not be able to be answered in a full meta analysis involving all studies on the mentally ill as this may end in a great deal of speculation.  However, a full meta analysis of all studies in all age groups could point these flaws out and lead to a more thorough study which would iron out those wrinkles.  I personally would look forward to seeing one.


Does a comparable metaphor exist for cognition that exists for slow & fast twitch muscle fibers? Skeletal muscles have slow and fast twitch fibers that differ in their rate of fatigue. Is there an analogue in the subject of cognition?
For example I might be very quick at doing coding but very slow at arithmetic. Also I might be fast at a mental task but tire quickly. What is the study of this phenomenon called?
Edit
It was suggested to me in a comment that the phenomenon of facilitation shows similar behavior.
Also mentioned in the comments is

system 1 "intuition" vs system 2 "calculation"

I would select it as an answer if it wasn't a comment.

It sounds like you are talking about system 1 and 2 thinking that Kahneman called'fast' and 'slow'.

While it's analagous to muscle fibre I'm not convinced it is as physiologically based.

System 1 is fast, but also characterised by its unconscious nature. The decisions made are automatic, and based on mental shortcuts or heuristics. It serves us well a lot of the time but is more error prone.

System 2 is more conscious and requires more cognitive effort. We are more likely to use it for complex decisions but only if we are aware of the complexity and consequences. It generally produces more reliable decisions.

You'll find the same concept with different labels, but the fast and slow thinking that Kahneman referred to is probably the best known.


Where can I find the connectivity matrix of the connectome of C. Elegans? I am trying to find the entire connectivity matrix for the connectome of the roundworm C. elegans. It is a much studied animal, as it features just a handful of neurons in its nervous system, 302 to be axact.

I've been looking forever and have come across this website that seems to have parts of the connectome (131 neurons and 277 neurons), but unfortunately it does not include the full connectome. In the Worm Atlas, under section 2.1 Connectivity Data, it says it has all the data, but it doesn't seem to have the adjacency matrix for the connectome.

If anyone can direct me to a source where I can find a connectivity matrix of the C. elegans connectome that would be a great help to me.

The full connectome of C. elegans (Fig. 1.) is described by Farber (2012) and as far as I know, the most complete data on C. elegans, including its connectome is available from the OpenWorm Project found here.

Fig. 1. C. elegans connectome. image source: Farber (2012)

Reference
- Farber, Sci Am February 2012

Further reading
- Are there organisms with fewer than 1000 neurons?


How many trials are needed to estimate a response time distribution? I want to estimate the properties of a response time distribution (mean, variance, tail-length) for individual subjects.

How many samples (trials) do I need to collect to get reliable estimates?

Does it depend on the method of estimation (i.e. maximum likelihood versus hierarchical Bayesian)?

Disclaimer: I'm not generally doing experiments where reaction time is the primary DV. But I thought I'd look at this issue and explored RTs from a neuroimaging dataset, and I think the findings are relevant to the question.

I think without further qualification, this question doesn't have an answer. Here I've plotted the estimation of reaction time/RT over the time course of an experiment (248 trials total), based on the RTs collected up to each time point, for a single subject:

For each point, the CI is the CI of the mean for all trials up to the respective trial number; so at x = 10, it's the CI for the mean based on the first 10 trials. Incremental mean is the mean over all trials up to this point; it is not the mean of means, but the mean of RTs. The total mean is the mean over all trials collected in this experiment.
I'm ignoring that the data is probably not normal for now.

As you can see, the width of the confidence interval of the mean asymptotes fairly quickly and doesn't get much better after 100 or so trials. However, you also see that the "incremental mean" (the mean of all trials up to this point) has not yet reached the true ("total") mean yet. This is likely because of a significant practice effect; the longer the experiment goes on, the faster the subject becomes. So while the precision of the estimate does not improve much after the 100th trial, the CI doesn't actually contain the "true" value- because the "true" value is non-stationary!
So maybe 200, 250 trials is not enough!? But I don't think the mean would have become stationary at a certain time point/trial count. Rather, eventually, fatigue would have overtaken the practice effect and RTs would have started rising again. d' would probably worsen, and variance rise, etc.
Metaphorically, we could call this Heisenberg's Uncertainty Principle in experimental psychology, in that we change what we measure by the process of measurement.

Now as you can see, this experiment is fairly special in that RTs are quite high - around 1500 msec. This is because my paradigm is comparatively complicated. Maybe practice would matter less, and the estimates asymptote more quickly, and more stable, in a different paradigm; for example, a very simple low-level signal detection experiment.  This is why I'm saying there is no straight-forward answer so far, as the specific behavior of RT depends on the paradigm.

Maybe you could try to account for the time effect - for example, with a regression with time as a predictor and estimation of the subject-specific intercept for RT independent of the time term. But then, that's "subject-specific RT intercept after removal of covariates" or something like that, not "reaction time mean".


How can automatic processing be estimated in an editing task? Is there a way of measuring/estimating the amount of controlled vs. automatic processes that takes place during a text editing task?

I know that asking participants to verbalise their actions and regard non-verbalised processes as automatic is a flawed approach. I came across the process-dissociation procedure, but this seems to refer to automatic/unconscious recollection after a learning task has taken place, and not automatic processes during the task itself.

Any suggestions of references or ideas on how to go about this?

What do you mean exactly with 'processes'? If you're thinking about actual movements made during editing (i.e. tiping), this science paper might help. Very simply put, they showed skilled typist have two kinds of control processes, one conscious and one unconscious.

(Science 29 October 2010:
Vol. 330 no. 6004 pp. 683-686
DOI: 10.1126/science.1190483)


Bias caused by the opinion of a famous person on matters they are not well-educated on? What is the name of the bias caused by the fame of a person on subject matters they are not experts on?

E.g: If a celebrity they like talks about climate change, people might tend to read, discuss, and follow their views as opposed to that of an educated climate scientist.

I don't believe that there is a cognitive bias that has been accepted by the scientific community that fits your fact pattern.  You can look for a matching cognitive bias yourself in this list:

https://en.wikipedia.org/wiki/Overconfidence_effect#Better-than-average_effects

I don't see one.  In fact, I don't even think people would believe a celebrity over an educated climate scientist on the current status of climate change.  It may help the person remember the ad or public announcement because a celebrity was the one to announce it but I doubt the credibility of the celebrity exceeds that of the scientist.


Does psychology lose it's validity when the subject is versed in psychology? Quite often, I find myself conforming to typical psychological principals, and exhibiting predictable behavior based on external stimuli. However, upon better research of the psychology behind past decisions that I've made, I become more likely to involve psychology theory in future decisions of the same kind.

But knowing the psychology behind typical decision making processes invariably changes the decision process you experience. It would seem that psychologists should be able to operate in a perfectly logical manner, however, as the saying often goes "All therapists are nuts!"

It's here I feel that traditional psychoanalysis fails. How can you apply psychology and analyze patterns in the thought process of a person if that person is versed enough in psychology to avoid traditional fallacies and pitfalls?

I would be especially interested to see any psychoanalysis studies done purely on psychologists.

There are two different traditions referenced in this question, psychoanalysis and decision making. If by psychoanalysis you mean the tradition of Freud and Jung, my understanding is that it didn't survive first contact with evidence-based practice and is now mainly of historical interest. Maybe some surviving approaches claim their roots in this, I'm not sure, I don't know much about the clinical side of psych.
I do know a little bit about decision making though, the other half of this question, and there knowing the psychology makes surprisingly little difference to people's decisions. You can learn to recognize a base-rate-neglect style question and memorize the answers to the CRT, which will put you in the minority ~20% who tend to get these kinds of questions right, but mostly decision biases are as compelling as perceptual illusions: even knowing that it's an illusion doesn't stop you from seeing the illusion in most cases.
The reason why is probably the same for both! Just like the visual illusions, it looks like many decision-illusions are not so much a flaw in the system as an artifact of how people deal with uncertainty efficiently and effectively using limited resources.

For more on this you might enjoy Kahneman's 'Thinking fast and slow' or Ariely's 'Predictably irrational'. These don't directly address the 'studies on psychologists' thing, but do give lots of examples of hard-to-unsee effects that most definitely persist after reading about them.


How distantly related are research in computational neuroscience and neural networks/machine learning? If one is more interested in understanding how algorithms in the biological brain solve problems (theoretically, particularly the mathematical aspect), and possibly in building brain-inspired computation (applied theory, particularly neurorobotics), then is it suggested to focus more on studying computational neuroscience rather than artificial neural nets/machine learning? It seems the latter one is more oriented toward any algorithms just to solve problems via computer simulations without the constraints of biological brains, though there are still large areas for theory of machine learning and artificial neural nets.

Computational neuroscience and neural networks are both studied on this MSc at the University of Sussex.
When I took the course in 2004/5, the Neural Networks module was compulsory, and the Computational Neuroscience was optional in the 2nd semester, so that would suggest the course designers (world leaders in biologically inspired computing) thought that studying neural networks first might aid the study of computational neuroscience.
I think some of the other subjects taught on the course would be of interest to you, e.g. evolving genetic algorithms for robot control (see Rodney Brooks – and the iRobot corporation).

Lastly to answer the question(!), I think you probably need some understanding of (simple) neural networks (artificial or otherwise) to understand more in-depth concepts in computational neuroscience.


How does recalling a specific memory decrease depression? Research by Serrano et al (2004) indicated that

  older adults with depressive symptoms showed that with increased
  specificity of memories, individuals show decreased depression and
  hopelessness and increased life satisfactions. - Wikipedia

Questions

Does the Seranno et al study  apply for most people?
How does recalling a specific memory decrease depression?
Can it be any specific memory?

References

Serrano, J. P., Latorre, J. M., Gatz, M., & Montanes, J. (2004). Life review therapy using autobiographical retrieval practice for older adults with depressive symptomatology. Psychology and Aging, 19(2), 272.

In a meta-anylysis, Bohlmeijer (2007) found that:

  In the last twenty years reminiscence has been applied in a large
  number of settings and with a large number of target groups. Examples
  of applications are: community-residents with a major depression,
  elderly with moderate depressive symptoms, nursing home residents,
  elderly with dementia, rural-dwelling older adults, elderly in
  assisted-living communities. ... We conducted a meta-analysis to
  assess the effects of reminiscence on depression across different
  modalities and target-groups. An over-all effect size of 0.84 (95% CI
  = 0.31 – 1.37) was found, indicating a statistically and clinically significant effect of reminiscence and life review on depressive
  symptomatology in elderly people. This effect is comparable to the
  effects commonly found for pharmacotherapy and psychological
  treatments. (p. 152f.)

To answer your first question, it seems that reminiscence and life review are an effective treatmtment of depression for a wide variety of (elderly) patients. It should be noted that a "significantly larger effect was found in studies in which life-review was the intervention (d=1.04) as compared to studies that used simple reminiscence (d=0.40)" (p. 152).

Several theories have been applied to try to explain how recalling memories decreases depression:

disengagement theory
ego-integrity theory
continuity theory
socio-emotional selectivity theory

Disengagement Theory

  The foundations for reminiscence and life-review therapy were laid by
  Butler (1963) in his famous paper The life-review: an interpretation
  of reminiscence in the aged. In this paper Butler put down his
  clinical observation of an increase of reminiscence – the act or
  process of recalling the past - in older people and postulated that
  this was due to the universal occurrence of an inner experience or
  mental process of reviewing one’s life. He conceived of life-review as
  a spontaneously or naturally occurring process that is ‘characterized
  by the progressive return to consciousness of past experiences, and,
  particularly, the resurgence of unresolved conflicts’ (Butler, 1963,
  pg 66). He hypothesized that it is caused by the ‘realization of
  approaching dissolution and death, and the inability to maintain one’s
  sense of personal invulnerability’ (Butler, 1963, pg 67). Though he
  recognized that people of all ages review their past from time to time
  and that any crisis may prompt life review, Butler stressed that
  life-review is more intensive and observed more frequently in (early)
  old age. He discerned adaptive and constructive manifestations of
  life-review from psychopathological manifestations. The adaptive
  variant is described as a reconsideration of former life-experiences
  and their meanings. It will often be accompanied by mild feelings of
  nostalgia or regret but is generally typified by expanded
  understanding and acceptance of one’s life, the experience of
  meaningfulness and declining death-anxiety. (Bohlmeijer, 2007, p.
  32)

Ego-Integrity Theory

  In its early stages reminiscence was studied mainly within the context
  of developmental stage theory (Erikson, 1963; Webster, 1999).
  Life-review was seen as a naturally occurring process which takes
  place in the last stage of the psychosocial development of human
  beings. The main hypotheses that could be deduced from this theory
  were that life-review is universal and old-age specific. These
  hypotheses were not confirmed in empirical studies. ... Based on
  studies rejecting the claim that life-review is old-age specific, it
  was suggested that reminiscence and life-review could be better
  understood within a life-span perspective (Webster & Cappeliez, 1993;
  Webster, 1999). ...

  In addition to the disengagement theory (Baum & Baum, 1980; Butler,
  1963) and the ego-integrity theory (Erikson, 1956; Taft & Nehrke,
  1990), in recent years new theories are applied to reminiscence, for
  example the continuity theory and socio-emotional selectivity theory.
  These theories fit with a contextual and life-span approach to
  reminiscence. (Bohlmeijer, 2007, p. 37f., 40)

Continuity Theory

  According to continuity theory individuals, when confronted with
  life-events or transitions, ‘attempt to preserve and maintain existing
  internal and external structures and they prefer to accomplish
  this objective by using strategies tied to their past experiences of
  themselves’ (Atchley, 1989, pg 137). This sense of continuity, with
  the aid of reminiscence, will promote adaptation (Parker, 1999).
  Continuity theory would predict that people will reminisce more
  frequently during periods of personal transition than in more stable
  periods. In testing this hypothesis, Parker (1999) found that young
  people were significantly more likely to reminisce during transitional
  periods than older adults. (Bohlmeijer, 2007, p. 40)

Socio-Emotional Selectivity Theory

  Another theory applied to reminiscence is
  the socio-emotional selectivity theory (Carstensen, 1995). This theory
  proposes that with growing age emotion regulation becomes more
  important than information gain and that the elderly arrange their
  social life in such a way (concentrating on close relationships) that
  they can have as many emotionally meaningful interactions as possible
  (Pasupathi & Carstensen, 2003). One important aspect of such
  self-regulation is known as the positivity effect (Carstensen &
  Mikels, 2005), in which it is assumed that an emo- tionally gratifying
  focus ‘...would bias attention and memory in favour of material that
  optimizes emotion regulation (i.e., positive material) even if there
  are costs to focusing only on such material’ (p. 118). This hypothesis
  has been supported by many studies (Kennedy, Mather, & Carstensen,
  2004).

  Older adults will therefore actively look for social
  interactions in which they reminisce because of the potential for
  emotion regulation and well-being (Penne- baker, 1997; Bluck & Levine,
  1998). This preference for talking about the past in social
  interactions with strangers was confirmed in several studies
  (Pasupathi & Carstensen, 2003). (Bohlmeijer, 2007, p. 41)

Note:

Bohlmeijer's dissertation gives a comprehensive overview of this area, if you want a quick introduction. It is available for free online (see link below). Serrano's article has been quoted 157 times, according to Google Scholar. Probably some of those articles will provide interesting criticism and more recent research not covered in Bohlmeijer's meta-analysis from five years ago. You can find these articles listed at Google Scholar.

Sources:

Bohlmeijer, E. (2007). Reminiscence and depression in later life (Dissertation). Am- sterdam: Faculty of Psychology and education, Vrije Universiteit. Available online at http://www.researchgate.net/publication/8958357_Effects_of_reminiscence_and_life_review_on_late-life_depression_a_meta-analysis/file/79e4151397c8674185.pdf


What are the possible causes of coulrophobia? Most sources on the internet say that coulrophobia is caused due to the unfamiliar face which often triggers fear to people (who suffer from it). What can be some other causes?

Coulrophobia is a fear of clowns.

It is a phobia not (yet?) acknowledged by the WHO or the APA as a disorder. Nonetheless it seems to be an accepted phobia in hospitalized children (Meiri et al, 2017).

The Guardian has a very interesting popular scientific account on the causes of coulrophobia. The author brings up the following two convincing arguments why clowns can be scary (and others arguments as well - I encourage you to read the article itself):

The “uncanny valley” effect: A phenomenon whereby things that look human, but are in fact not quite human appear as highly unsettling. Think of a dead body for example. In case of a clown their elaborate make up and weird behavior contradicts our sense of 'normal'.
Unpredictability is something which causes distrust and apprehension in humans. Clowns are by their very nature unpredictable, as they always act weird and do not adhere to social standards.

Reference
- Meiri et al., Eur J Pediatr (2017); 176(2):269-72


Calculate threshold from 'binary' yes/no data For various reasons, I have a crappy experimental design that I am forced to deal with. I present subjects with 20 yes/no trials, out of which 5 are no-signal catch trials and 15 are signal trials. Each signal presentation has a unique level with unequal spacing (as small as one in arbitrary units and as great as 5). All subjects run the trials in the same order (i.e., the 5th trial is always at signal level, and the 11th and the 6th trial are always catch trials).

To make things more complicated, at the population level, and likely at the individual level, the criterion is not stable such that the probability of saying yes on a no-signal trial depends on the catch trial number (the 1st catch trial has a probability of yes of about 0.05 and the 5th catch trial has a probability of yes of about 0.2). From this mess, I need a single number representing threshold. I don't really care what the threshold corresponds to (e.g., the signal level leading to 50% yes, 50% correct, or a d' of 1 would all be fine). Ideally, the method would provide a confidence interval on the estimate at the individual subject level.

I was thinking of using a Spearman-Karber type approach, but the unequal step sizes seems problematic (along with the variable criteria). I also don't understand the history of Spearman-Karber (i.e., where was it first published and how it relates to Spearman 1908) and kind of hope that maybe in the past 100 years we have improved on things.

The biggest drawback of your procedure, also point of discussion previously here is the limited number of trials. Apparently, you obtained binary data, namely one answer (yes/no) per trial, basically leaving you with a sparsely sampled, binary data set. Binary data will not allow a curve fitting, which is the conventional way to determine a threshold.

To make matters worse, there is a certain bias in the catch trials. But values anywhere below 25% false positive are, imo fine. So let's forget that issue, as it is likely the least of your problems.

Now, single-stimulus per trial data are referred to as the Method of Limits. Basically what you would normally do to obtain a threshold with MoL is increase the level to see where the subjects starts perceiving the stimulus (YES/NO reversal) and then flip the sequence and see where the person stops answering YES and hits NO. Generally, such a procedure is experimentally used to get a quick handle of a good starting point for the 'real deal' experiments. Or, it is useful in clinical environments. For example, clinical audiometric thresholds are often determined this way - quick and dirty, but accurate by about 5 dB or so.

The response you get in this case is a so-called type 2 response, since you never can tell whether the subject was right or not. You just evaluate when the subject reports to perceive the stimulus. The problem with the method described here is that the S may become habituated (I didn't perceive it now, likely I won't in the next trial) or the S makes the error of expectation (It will probably become apparent now).

The only way in which I can see to analyze your data is determine the flipping point and take that as a measure. You can then, perhaps take the average between the two intensities where the response flips to get an estimate of the 50% level, the gold standard of the threshold in yes/no tasks.
Likely you will not have an unambiguous flipping point in your data, but I'm sure you can think of something. Perhaps just take the lowest intensity where a flip occurred, or something along those lines.
Alternatively, you may group your intensities into approximate levels and average out the responses to get values including rates between 0 and 100%. This procedure, however, is likely pretty much doomed to be shot to pieces by any referee or peer in your field, the more since your step sizes are unequal.

Reference
- Kingdom & Prins. Psychophysics. Elsevier 2010


What is the neurobiological basis of the "inner voice" used for thought or reading? I've recently experienced a number of hypnogogic near sleep states characterized by change in thinking (stage 1-2 sleep). I noticed that if I let go and get absorbed in the state, I can follow it.

I can describe the hypnogogic sensation as a feeling of empty space without a definite boundary. Typically the state arises at 17-23 minutes after bedtime (I'm using a timer to check). However, as soon as I activate "inner voice" or think a thought spoken in that voice, those other near sleep states get completely suppressed. Literally, a single word disrupts these states.

This makes me interested what happens in the brain when a person thinks using a single threaded, spoken train of thought? ("I'm typing a question on cogsci right now" or "I'm reading a question right now") Is there some part of the brain that gets activated while others get suppressed? In particular I'm interested why spoken thought suppresses other non-verbal states that a brain can consciously experience?

  Internal monologue, also known as inner voice, internal speech, or
  verbal stream of consciousness is thinking in words. It also refers to
  the semi-constant internal monologue one has with oneself at a
  conscious or semi-conscious level.

It would be interesting to know if there's some difference that fMRI can show between a brain that's reading using voice and brain that's reading non-verbally.

I recall reading about similar phenomenon in the eastern spiritual traditions, like Taoism or Buddhism, where the states of mind they are trying to achieve are also incompatible with inner voice.

Preliminary answer I intend to improve later. Stumbled upon this in the context of description of how people read:

According to this paper on readin (Sousa, 2005), novice readers internally verbalize written words of English and German using "an area of the brain just above and behind Wernicke's area". This area then communicates with the Broca's area and the frontal lobe.

Found this additional article which mentions that people use the same area of the brain when reading silently as when listening actively.


How are qualia localized in consciousness? I understand that evolution incorporated arbitrary qualia into the default network to inform consciousness (the largest cranial global processing information subnetwork) about properties and qualities of the body in spacetime. However, how does the feeling in my toe know to appear near my toe when nerves there are stimulated? Is this an illusion, and there is extraneous processing that matches the visual stimulus of me looking at my toe and the tactile stimuli of someone touching it to make those qualia feel related, even localized in the same area in space?

What if my somatosensory cortex was moved to my stomach (say all dendrites and axons were chopped off and were replaced with wireless hubs that signaled to the newly transplanted somatosensory cortex in my stomach). I would presumably experience no change in consciousness, which indicated localization of qualia is not achieved by the spatial embedding of the neurons, but by their graph-theoretic interconnection.

If I swapped the information processing (in some information-theoretic sense, say graph-dynamics) associated to the smell of strawberry (it's much more complicated than that but just go with it for a second) with the brain's processing of thermal information from afferent skin sensors, would I appear to feel the smell of strawberry all over my body when it's cold and the feel of cold in my nose when I smelled strawberry? I am excluding affect swap here so the qualia of strawberry smell now feels unpleasant like cold and the qualia of cold feels pleasant like strawberry smell.

Now what if in mad science I permuted the thermal sensors all over my body? Say my foot and hand neurons got swapped (say through a nanobot intercepting wireless relay). Would my hand feel cold when my foot is immersed in ice and vice versa? This would indicate these qualia are processed in consciousness in the brain rather than at the afferent sensor sites.

For bonus credit: How does this relate to phantom limb syndrome? Are there other observed processing defects that lead to faulty localization? E.g. Out of body experiences, certain particularly nasty mental disorders like dementia, rewiring of somatosensory map due to stroke, that engineering dean who wanted his arm chopped off (I forgot the name but I heard this from V.S. Ramachandran)

Second bonus credit: I've read "butterflies" in your stomach are serotonin releases in the enteric nervous system. Doesn't consciousness have to be informed of this release for you to feel it? If not, how do disconnected information graphs allow you the cohesive ability to feel in love?

This question has been unanswered for a long time and I will attempt to address the issues posed not one by one, as there are a great many questions, but with an overall working of the sensory nervous system with respect to topographic mapping. Moreover, the question uses a great many "suppose ifs" that have never, and most likely will never or cannot be tested. Therefore a basic overview of topographical mapping may shed light on the matter.

The somatosensory cortex is a highly topographically organized structure. Although warped in size, it basically contains an exact topographical map of the body, referred to as a homunculus:

Source: Guardian

In other words, perceptions in the upper arm are represented very near to the lower arm representation in the somatosensory cortex. The motor cortex contains a very similar map.

Similarly, the visual cortices contain many maps representing the visual field, referred to as the retinotopic map. Likewise, the auditory system maps frequency space in a highly topographical manner (the tonotopic map).

Removing a part of the somatosensory cortex out of its context may wreck havoc on this ordered structure. For example, it has been shown by groundbreaking work from Michael Merzenich and colleagues that when the fingers of a monkey are sewn together, the finger representations in the sensory cortex also fuse, i.e., the border between the coupled fingers degrades and vanishes eventually. This experiment shows that when two separate bodily structures are repeatedly and structurally stimulated simultaneously, they fuse in the cortex. Upon separation, original mapping is restored (Allard et al., 1991). I consider this proof that adjacent structures influence each other's representations in the cortex because they often receive parallel stimulation. Coherent stimuli typically result in increased synaptic strength.

Phantom limbs are interesting indeed. For example, the groundbreaking work by Ramachandran focused on upper arm amputees. These folks would feel sensations in their (amputated) hand when their cheek was stimulated. In the homunculus it can be readily seen that facial representations are close to the hand representation. Upon deafferentation of the arm region in the cortex, surrounding bodily representations take over the 'silenced' regions, and the cheek region 'steals' the hand (which is relatively huge). However, interestingly, the cheek not only serves its own original representation, but refers now to the amputated hand as well. Hence, the memory of the hand lingers, showing once again that the bodily map is strongly imprinted in the brain and that it is not simply isolated from its context.

How then are visual and tactile stimuli fused as being correlated? This happens in the higher multi-sensory areas in the brain, the so-called association cortices such as found in the temporal lobe.

Source: Insituto Balseiro

These higher areas will link various perceptions and merge them into coherent perceptions. Limbic association areas may couple the butterflies to love.

Conclusion
In all, qualia are localized in the brain by mapping sensory information onto highly organized topographic maps in the cortex. Changes in the periphery (e.g. amputations) will affect this cortical mapping due to plasticity and hence these cortical maps are plastic (subject to change). The reverse can never be easily tested (taking a piece of brain away will have gross consequences) as said, but I think that the quote "Neurons that wire together fire together" is important here. As said, synaptic strength increases when adjacent neurons fire in coherency and when taken apart their mapping will become distorted. Lastly, emotional feelings are combined with the physical sensation of butterflies in your stomach and synthesized into a holistic feeling of love, probably by the limbic association cortices and perhaps other association areas. in general, the association areas synthesize the various sensory systems by linking them, most likely due to experience.

Reference
Allard et al., J Neurophysiol 1991;66:1048-58


ML/Neuroscience: TensorFlow vs PyTorch vs Keras for bulding NN models of the nervous system? I would be very grateful to people with experience in using neural network models in neuroscience for advice!

What approach would you recommend for building neural networks?

I am choosing between TensorFlow, PyTorch and Keras. An important aspect for me is to be able to easily access the params of the NN (especially the weights). I want to build encoding models of biological neurons so for me model transparency, interpretability and exploration capacity is as important (if not more) than performance metrics or efficiency.

Thanks!

If you want to build a neural network as a biological simulation, maybe none of these are the best options, since they are more suitable for deep neural networks. If you want to mimic synapses using some model as Hodgkin and Huxley, you must use some different approaches. For that, you may use NEURON environment (https://neuron.yale.edu/neuron/), which has some implementations of the theoretical models behind action potentials. It comes with a gui, but personally I don't like it, so I just code everything using their python's library.

On the other hand, if you are just looking for a way to model a network, without adding too much complexity, then any of your examples are probably are ok to build directed graphs.


On what basis do professionals who recognize gender dysphoria support risky and permanent medical intervention for those seeking gender re-assignment? Before I pose my question, here are some statements from a slideshow on "Understanding Gender Nonconformity in Childhood and Adolescence" by Robert Garofalo, attributed to the Children's Hospital of Chicago, and hosted by the American Academy of Pediatrics (AAP). They officially support affirming gender change in children, however there is a group of pediatricians who actively reject that position.
According to this slideshow, gender is a social construct (page 7), which "[v]aries by place, time period" .
Next I'd like to list the slideshow's listed side effects and irreversible effects of hormone therapy. Pages 39-41 show the side effects of testosterone therapy.

Irreversible Effect of Testosterone Therapy

Lower voice pitch
Increased hair growth (arms, legs, chest, ab)
Mustache/beard growth
Male pattern hair loss (temples, crown) and possibly baldness
Genital Changes
Genital changes (clitoral
growth and vaginal
dryness/fragility)
Fertility?

Side Effects/Risks: Testosterone

Increased cardiovascular risk

Increased weight
Decreased HDL, Increased Triglycerides
Increased BP

Increased insulin resistance
Hepatotoxicity
Mood changes: irritability, aggression
Headaches
Acne
Polycythemia
Theoretical risk: breast/endometrial cancer

Given these side effects, on what medical basis do health professional support this?
If a person doesn't like themselves they get help with their self-value.  They learn the valuable things about their unique identity and also identify why they began to devalue themselves and deal with those root issues. People with phobia's are taught to manage and improve their phobia, not embrace it.
My point is not to compare one disorder to another, but to show that regardless of the type of disorder that the standard treatment is not acceptance, but rather to reveal deeper issues and otherwise manage and overcome the disorder.
Gender Dysphoria is treated categorically different, but there has been no new category defined on which to base that decision.
I know this is a sensitive topic and has many personal stories, but I'd like to focus on the professional medical position and reasoning for that position.

I hope I am qualified to answer this question. I am not a psychologist but have worked with transgender persons in volunteering positions a number of times and am fairly well researched on the topic.

The biggest key point as I have studied simply is based on health outcomes as opposed to comparing this to mental illness.

This page talks about the practical health outcomes of the treatments. Individuals who identify as transgender already often suffer from a variety of issues that reduce both their quality of life and in some cases health. These can include developing mental disorders if they do not get treatment and even self harm or suicide. Overall most of the linked studies in that article showed that the benefits largely outweighed the risks in an overall health decision.

Now you imply that other treatments are used for most conditions which have effects on mental health, usually either "talking cures" or medications. The difference being in almost all cases these treatments are ineffective or even make the situation worse in transgender individuals.

I cannot find a study to link to this which is publicly available right now but in short, treating transgender individuals with treatments used for mental illness usually makes the condition worse. In many cases it causes additional depressive disorders to form as well as long term self image problems and self hatred, as well as increasing the risks of self harm or suicide.

So in summary, it is not to say the treatments used for transgender persons are risk free, but merely that they are better than the alternatives both of doing nothing and of trying to use a purely psychiatric method to treat. As both of those tend to make the condition gradually worse and no other treatments are known which produce a consistent improvement.


Why can some drugs make us hallucinate and think the hallucinations are reality? The question above mainly applies to dramamine. I've only taken 1 tablet for carsickness, but I have read about experiences with that drug. I'm including other drugs that can make you hallucinate and think it's real.

Furthermore, why can you still see the hallucinations as reality if you affirm to yourself that the things you see aren't real?

In my opinion this has to do with how perception works in general.

There are many situations, where you "see" something, that is not there. Optical and other sensory illusions are a prime example. Usually these mis-perceptions result from sensory input that our organs of perception were not built to analyze. For example, the size-weight illusion stems from the fact that we don't have objects of equal size and equal outside material but differing weights in our natural habitat. You will easily recognize that all sensory illusions are induced by highly artificial stimuli such as straight and parallel lines, which have only existed in the most recent past and have as yet not had a big influence on human evolution.

In the case of drugs and hallucinations, your brain is stimulated in a way that is not meaningful for it, and it tries to make sense of what if "perceives" in the context of its evolution and experience. Obviously the stimulation by a certain drug comes close to what the stimulation would be like if outside reality were like you hallucinate it.

A drug induced hallucination is basically a sensory illusion, with the difference that you stimulate the brain directly, instead of the sensory organs.

To "break" an illusion, you need to provide a stimulus that overrides or "corrects" the misperception, e.g. a ruler to show that the lines are parallel (or not parallel) etc. Just knowing the truth (because you drew the lines yourself) doesn't change the effect.

Since drug induced hallucinations originate not in an outside sensory stimulus but in a direct manipulation of the brain, I would guess that touching the elephant head of your friend might not help to break the illusion -- you might even feel differently. But I have no experience with drugs and couldn't find any reports on this.


What is the fear/paralysis that occurs before doing an irreversible action? I often experience paralysis in the face of an irreversible decision or action. What is the term for this or what is it that I'm looking for to describe it and/or research it?

Some examples of this feeling:

Leaving for a trip: if I forgot something, once I'm at the airport it'll be too late to go back
Throwing a garbage bag in a dumpster: if I dropped my phone in the garbage at some point, I'm never getting it back
Dropping a bundle of letters into a mailbox: if I got someone's address wrong, I can't just reach in and pull the letters back out
Buying something without a return policy: if I don't like it, I'm never getting that money back
About to jump out of a plane (e.g., skydiving): if I don't like the feeling, I can't just hop back on the plane immediately

I was listening to a podcast in which this was referred to as the "call of the void". However, the (not) ever-reliable Urban Dictionary describes the call of the void as the "what if I jumped" thought, which seems different somehow.

This question is related to (but I think not a duplicate of) the Paradox of Choice, which, as I understand it, states that when people are given more choices, they tend to have difficulty making the decision and are often dissatisfied with the choice they made. It seems this anxiety I'm describing has more to do with the irreversible nature of the decision or action.

Philosopher Walter Kaufmann calls this fear "decidophobia", but I have never read and cannot find any psychological publications using that term.

If you think about the phenomenon, it becomes apparent that anyone can clearly observe when a person hesitates to decide, but even that person herself could probably not clearly identify all the emotions that accompany this behavior, and, if there is fear, what the exact object of that fear is – the fear could be of anything from deciding between two equally desirable alternatives (fear to decide) to the outcome of a decision that is in fact already made (fear to finalize the decision and face the results).

Psychology therefore prefers to study observable behavior and calls this behavior "decision avoidance".

The above answers the question you asked in the title of you question. Your post itself describes a bundle of symptoms that to me are reminiscent of what persons with obsessive-compulsive disorder experience. Many such disorders begin with a worry that something was forgotten and lead to extended rituals of checking for hours if the water is turned off or the lights are out. The problem here is that these people become increasingly incabable of trusting their perceptions and have to repeat certain actions until they are finally convinced the thing was done.

An example is of a woman who frequently goes on business trips and, upon returning home, has to read the name of her city several times loudly letter-by-letter at the airport to get the feeling that she is actually there.

Since I know nothing about you beyond your post, your problem – if it is one – is hard to diagnose. If this "fear to decide" affects your well-being, I recommend you go see a psychologist and talk to them about it.


Is it better to say "Don't forget" or "Remember" in written encouragement? This is more of a subtlety and goes beyond general English Language & Usage and is more about the cognitive process surrounding the use of language.

It seems like I heard once that, while it is common to say, using a phrase like "Don't forget" or "don't miss" is essentially a cognitive double negative. Consciously we understand that "Don't forget" means to "remember" but unconsciously our minds drop the "don't" and file it as "forget," thus conveying the opposite message.

The argument goes that if I tell you "don't think of a pink elephant" then you need to first think of the pink elephant before you can cognitively not think of it. Later if you recall back to the conversation you would remember it was about pink elephants and not thinking of them.

I'd argue that Churchill's "Never,  never, NEVER give up" didn't reputedly have this effect.

With 'Don't forget' the 'don't' may well outweigh the infinitive verb in its cognitive effect, especially if stressed. The language here is of stimulation, incentivising, or command, and I'd say the more likely undesired reaction is the dislike of the perceived patronising (or, certainly, the imperious) approach.

With 'Don't think of a pink elephant' there is little likelihood that one feels patronised or browbeaten.


Why do humans have sex in private? Human couples usually have sex in private, hidden not only from predators, but also - other humans. It is unlike behavior of most species, including our relatives: bonobos, chimpanzees and gorillas.

Is private sex mostly a biological or cultural behavior? What is the advantage (if any) of such behavior?

Introduction
It is interesting and quite under-researched topic in psychology. What has been studied and definied extensively are different abnormal sexual behaviours, and exhibitionism is one of them. In the DSM-IV exhibitionism is defined as sexual arousal by revealing one's body or performing sexual acts in public and it's a form of paraphilia. Attraction to being watched by others during  sexual intercourse is a form of exhibitionism called martymachlia. Presence of such sexual behaviours in DSM-IV is a clear indication that majority our society have deeply enrooted social and moral norms regarding inhibition sexual behaviour in public. If you think about it, majority of countries bans public sex and limits exhibitionism to designated places (nudist beaches and nudist colonies).
EDIT
Following valid and constructive comments by @Piotr and @Preece I removed speculative part of my answer about cultural factors and expanded my answer arguing for evolutionary explanation.
Territorial mating behaviour in animals
Initially I should point out that you are not exactly right in saying that 'most species don't practice private sex'. It's true that many primates do that. But we can argue that some territorial behaviours in animal kingdom are a form of providing security during mating. Those behaviours are very common in animal world including lizards (Davis, 1980), birds (Brown, 1969; Greenwood, 1980) and mammals (Greenwood, 1980).
Evolutionary development of shame
@PiotrMigdal specified that he is mainly interested in the issue of "unwillingness to have sex in public". We can trace the origin of such 'unwillingness' to the sense of shame that could be explained from evolutionary standpoint. Darwin (1872) argued that shame represents what would be at the primitive level an instinctive seeking for cover, but his elaboration on this wasn't clear. MacCurdy (1930) took this idea further. He argued that prehistoric man sought concealment for activities which expose him to danger in a hostile environment, e.g., eating, sleeping, sexual intercourse and excretion (Maccurdy, 1930). Concealment was sought prior to the fulfilment of any act that would limit or prevent rapid self-defence. For example, Maccurdy (1930) boldly pointed out that postures during both sexual intercourse and excretion prevents people from rapid self-defence.
Malinowski (1927) writes that:

it is characteristic that sexual activities, sleep and excretion are
surrounded by protective taboos and mechanisms of concealment and
isolation in almost every society.

In this context, the sense of shame could have developed as a response to natural drive for self-protection (Dawrin, 1872; Maccurdy, 1930). Therefore, evolutionarily this would form the basis of unwillingness of having sexual intercourse in public.
Because personal security increased with the development of civilisation, the sense of shame has also transformed and became more sophisticated (Maccurdy, 1930). The shame exists only for specific situations (e.g. public sex), but it doesn't apply in other social conditions. Maccurdy (1930) gives examples with excretion, where it isn't uncommon for partners to urinate in each others presence or in the presence of other friends. We can also put nudist beach in this 'shame-exclusion' category. Overall, evolutionary account would highlight that out need for private sex is related with growth for security, the extension of shame, and the evolution of modesty. Along the same line, Malinowski (1927) also points out that sexual intercourse in public could excite jealousy and would be an indicator to invite rivals to seize that which is being enjoyed.
References:

American Psychiatric Association. (2000). "Diagnostic and statistical
manual of mental  disorders" (4th ed., text rev.).
Davis, J. (1980) "The times of mating and oviposition of the Western
fence lizard S.o.occidentalis", J. Herpetol. 14:102
Brown, J. (1969) "Territorial behavior and population regulation in
birds: a review  and re-evaluation". Wilson Bull. 81:293-329.
Greenwood, P. J. (1980) "Mating systems, philopatry and dispersal in
birds and mammals."  Anim. Beha. 28, 1140-1162.
Darwin, C. (1872) "The Expression of the Emotions in Man and
Animals." London: John  Murray.
MacCurdy, J. (1930) "The Biological Significance of Blushing and
Shame." British Journal  of Psychology, 21, 174-182.
Malinowski, B. (1927) "Sex and Repression in Savage Society." London:
Kegan Paul, Trench,  Trubner & Co.


At what age a child would develop a sense of racism or a minority discrimination? I wonder if what happened with my son(6yo) is a matter of concern or just a coincidence.

I think I need to give a bit of background to help analyze what happened.
We are an Arab family live in the UK, majority of my town is of European/Caucasian ethnicity, although there are few Arab families we know about, but we don't really communicate much.
He is the only student who speaks Arabic in his class (there are Polish and maybe other European languages), I don't know about the rest of the school, but if I guess, there isn't in this school.

Me and him were in the car, I was looking for a place to park, and just went by a car park but it wasn't available for normal parking (contract parking).
I said: We can't park here.
He said: Why? Is it because we speak Arabic?

At the beginning I laughed, and told him there is no such thing, but couple of seconds later I was wondering, how would he develop such idea?

I know this might sound like a troll, but I swear that what really happened, and I am concerned if my son is facing any acts of racism/discrimination, maybe in the school.

Children as young as two to three years old are able to pick up on racial categories and stereotypes, and to infer that others' behavior is driven by race (also gender and other categories).

Of course, at that age children are actively exploring causes in the world of all types, so a comment asking about Arabic language does not mean that a child is experiencing extensive discrimination due to race - on the other hand, I think it would be naive to think anyone with any minority characteristic is not experiencing any discrimination ever, especially in comments from other kids who are themselves learning about the world and other people. It also could have been something overheard on TV, it could have been from a discussion of discrimination rather than an experience, etc.

Corenblum, B., & Annis, R. C. (1993). Development of racial identity in minority and majority children: An affect discrepancy model. Canadian Journal of Behavioural Science/Revue canadienne des sciences du comportement, 25(4), 499.

Hirschfeld, L. A. (2008). Children’s developing conceptions of race. Handbook of race, racism, and the developing child, 37-54.

Katz, P. A., & Kofkin, J. A. (1997). Race, gender, and young children. Developmental psychopathology: Perspectives on adjustment, risk, and disorder, 21, 51-74.

Pauker, K., Ambady, N., & Apfelbaum, E. P. (2010). Race salience and essentialist thinking in racial stereotype development. Child Development, 81(6), 1799-1813.

Taylor, R. G. (1966). Racial stereotypes in young children. The Journal of Psychology, 64(2), 137-142.


Can hypomania be induced by just thinking quickly and variably? Emily Pronin and Daniel Wegner have shown that fast and variable thinking induces positive affect. This is independent of thought content. Sheri Johnson has noted that the key things that might start a hypomanic/manic episide are a night of no sleep, a positive life experience, and certain drugs.

Is it possible to clinically induce hypomania by just thinking quickly and variably?

Note that an easy exercise to implement this would be to think of a word and then a word beginning with the previous word's letter.

Added. In a sense, the above exercise is "anti-meditation." Mindfulness is essentially low thought speed combined with high variability. The ideal state would be high thought speed and high variability.

References

Pronin, E., & Wegner, D. M. (2006). Manic Thinking Independent Effects of Thought Speed and Thought Content on Mood. Psychological Science, 17(9), 807-813.

I had a read through the Pronin and Wegner study.
The study had a sample size of 144. They manipulated thought speed by getting participants to read aloud one statement after another at either half normal reading speed (slow thinking) or double normal reading speed (fast thinking). They also manipulated the content of the text being read (depressing statements versus elated statements). They seemed to find that both the content and the speed of thought manipulation seemed to yield similar increases in positive emotion, energy, feelings of power, feelings of creativity, and grandiosity.

The first issue is whether their study is replicable. I don't know the literature regarding replications, but all the effects seem plausible, and the sample size is reasonable for this kind of study.

Another issue is how the manipulation of reading speed affected the reported emotions. Perhaps the slow reading led to frustration or being annoyed.

With regards to the nature of the effect, there are questions of how long this mood induction lasts. My guess is that the effect of the mood induction would be short lived.

There is also a difference wherein mania the speed of thought is presumably internally driven whereas on this task the "speed of thought" is externally driven. The study did not measure whether this "speed of thought" continued after the external stimuli was removed. For example, does speed of thought work with an inertial principle or not such that it can be started with external stimuli and will keep going on its own. My guess would be even if such a concept of inertia existed, people would quickly return to their own typical level. Thus, I don't think such a manipulation would induce clinical levels of mania, especially not in a sample of participants who do not suffer from bipolar disorder.


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

Are there references to the literature?

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

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

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


Study claims that human brain does not produce new brain cells? Neurogenesis is one of the most fascinating subjects to discuss. However, it seems like scientific community has difference of opinion about whether neurogenesis is possible or not in adult humans. The aim of my question is to gain insights about whether neurogenesis in adult humans is possible or not.

According to an article presented in Scientific American "The Birth of a Brain Cell: Scientists Witness Neurogenesis", Mirjana Maletic-Savatic, an assistant professor of neurology at Stony Brook University in New York State, claims that neurogenesis is possible. Her study is based on brain imaging and suggests that scientists "witnessed" neurogenesis and the birth of new brain cells in adult human brain.

However, on the other hand, there is a Californian study, reported on in ScienceNews "Study casts doubt on whether adult brain’s memory-forming region makes new cells", that claims that neurogenesis in adult humans does not exist.

Analyzing the study contradiction

These two studies contradict each other. One may try to reconcile these two studies by claiming that humans only produces new cells in only certain parts of the brain but not in other parts of the brain, including hippocampus. Hippocampus may not be able to produce more brain cells, but other parts of the brain may generate new brain cells. However, this explanation and the above mentioned study directly contradicts another study that was published by Berg D.A. et al., 2013:

  active adult neurogenesis is confined to two distinct locations: the
  subventricular zone (SVZ) of the lateral ventricles in the forebrain;
  and the subgranular zone (SGZ) of the dentate gyrus (DG) in the
  hippocampus

We can see that the Californian study contradicts the other study clearly when it comes to studying and analyzing neurogenesis in the hippocampus.

The question

This theory and the Californian study does not explain why people who suffer from memory loss in some parts of their lives regain memory and perform much better on memory tests.

If the hippocampus does not make new brain cells, then how do people regain memory by eating the right diet and exercising? Is neurogenesis possible in the hippocampus region of the brain?

Berg, D. A., Belnoue, L., Song, H., & Simon, A. (2013). Neurotransmitter-mediated control of neurogenesis in the adult vertebrate brain. Development, 140(12), 2548-2561.

The hippocampus does make new brain cells, especially after aerobic exercise; there is an overwhelming amount of evidence for this claim (Erickson, Voss, et al., 2011; Firth, Stubbs, et al., 2017; Patten, Sickmann, et al., 2013). I was unable to find the California study published or peer-reviewed anywhere, and the abstract presented at the conference contained no indication of the sample size used in the study or a justification for why those specific types of neurons were studied. Therefore, it is unclear whether this single study was correctly conducted, and the article discussing the abstract is appropriately cautious about interpreting the results.

There's many different reasons why this study might contradict the scientific literature on hippocampus. One might have to do with a neurogenesis marker they used, doublecortin (DCX). One study notes that DCX levels may be dependent on specific brain regions and can be affected by age, although this is uncertain (Balthazart and Ball, 2014). Another study also warns that DCX reading levels should be interpreted with caution because they can exist at relatively high levels outside of neurogenesis (Kremer, Jagasia, et al., 2013).


Is getting trapped in an asylum a realistic scenario? In various movies, most recently Unsane (2018), a scenario is painted in which a healthy person gets committed and trapped in an insane asylum and the caretakers there are more or less indifferent to whether she is actually sane or not.

In the movie she "voluntarily" commits herself by signing a form, so presumably she will not be afforded the protections some states give to involuntarily committed people.

Is this scenario realistic in the United States? Can a person who "voluntarily" commits themself, be turned into a medicated prisoner with no recourse for freeing themself?

It all boils down to the Duty of Care

Duty of Care

The duty of care is the responsibility of a mental health professional to protect patients and others from foreseeable harm. If a client makes statements that suggest suicidal or homicidal ideation, the clinician has the responsibility to take steps to prevent harm where reasonably practicable, and if necessary, initiate involuntary commitment.

The same goes when a person has been assessed as suffering from one or more severe mental health conditions which has a high chance of resulting in any other physical harm to the individual or others.

Voluntary Commitment

Getting committed either voluntarily or involuntarily is not straight forward.  In both the US and here in the UK, you can't just go into a hospital, sign a form and then be taken in as a mental health patient.  You can go into a hospital and ask to be committed, but you need to be assessed in order for the committal to be accepted.

Involuntary Commitment

With voluntary committal, you are free to discharge yourself by signing a discharge form and leave at any time, however, if at any time it is deemed that you would be a danger to yourself or others, the voluntary committal can change to involuntary committal.

Aside from an unscrupulous group of psychiatrists it is practically impossible to trap a mentally healthy person in a psychiatric unit against their will.  For a person to be held against their will, it needs the co-ordinated efforts of more than one psychiatrist.  Where it happens that a mentally healthy individual is held against their will, there is possible legal redress and the psychiatrists involved could have their practice licenses removed.

In the US

Voluntary Committal

As pointed out by psychiatrist, Scott Alexander, in his Slate Star Codex post, you are not guaranteed admission to a psychiatric unit on a voluntary basis just because you want it. You might be turned down if the psychiatrist thinks you aren’t sick enough to need it, or if your insurance refuses to pay for it. Insurance companies are very reluctant to pay for hospitalisations unless there is a clear risk involved.

Involuntary Committal

The laws governing this seems to differ depending on which state you are in.

For example:

In CaliforniaAccording to the Lanterman-Petris-Short Act (Section 5150 of the California Welfare and Institutions Code)

  When a person, as a result of a mental health disorder, is a danger to others, or to himself or herself, or gravely disabled, a peace officer, professional person in charge of a facility designated by the county for evaluation and treatment, member of the attending staff, as defined by regulation, of a facility designated by the county for evaluation and treatment, designated members of a mobile crisis team, or professional person designated by the county may, upon probable cause, take, or cause to be taken, the person into custody for a period of up to 72 hours for assessment, evaluation, and crisis intervention, or placement for evaluation and treatment in a facility designated by the county for evaluation and treatment and approved by the State Department of Health Care Services.

In FloridaAccording to the Florida Mental Health Act

  A person may be placed in involuntary inpatient placement for treatment upon a finding of the court by clear and convincing evidence that:

  (a) He or she is mentally ill and because of his or her mental illness:

  1.a. He or she has refused voluntary placement for treatment after sufficient and conscientious explanation and disclosure of the purpose of placement for treatment; or

  b. He or she is unable to determine for himself or herself whether placement is necessary; and

  2.a. He or she is manifestly incapable of surviving alone or with the help of willing and responsible family or friends, including available alternative services, and, without treatment, is likely to suffer from neglect or refuse to care for himself or herself, and such neglect or refusal poses a real and present threat of substantial harm to his or her well-being; or

  b. There is substantial likelihood that in the near future he or she will inflict serious bodily harm on himself or herself or another person, as evidenced by recent behavior causing, attempting, or threatening such harm; and

  (b) All available less restrictive treatment alternatives which would offer an opportunity for improvement of his or her condition have been judged to be inappropriate.

In the UK

The whole issue of committal, voluntary and involuntary, is governed by the Mental Health Act 1983 and the Mental Health Act 2007.

Involuntary Committal in the UK

To be involuntarily committed (also known as sectioned), it needs to be founded on the written recommendations in the prescribed form of two registered medical practitioners, including in each case a statement that in the opinion of the practitioner:

The individual is suffering from mental disorder of a nature or degree which warrants the detention of the patient in a hospital for assessment (or for assessment followed by medical treatment) for at least a limited period; and
The individual ought to be so detained in the interests of his own health or safety or with a view to the protection of other persons. (See Sections 2 and 3 of the Mental Health Act 1983)

For voluntary committal in the UK

It needs to appear to the registered medical practitioner or approved clinician in charge of the treatment of the patient that an application ought to be made under Section 5(2) of the Mental Health Act 1983, for the admission of the patient to hospital, he or she may furnish to the managers a report in writing to that effect; and in any such case the patient may be detained in the hospital for a period of 72 hours from the time when the report is furnished. By which time the patient should be assessed by the two registered practitioners prescribed in Section 2 of the Act.


What is the difference between emotions, intuition and affect? From what I know, intuition is affect-based. But how do they differ?

Affect is a fundamental feature of consciousness and is a mental representation of input from the body to the brain.  Affect corresponds to feelings of (un)pleasantness and activation (arousal).

Emotions are conceptualizations (interpretations) of your affect in a given context.  You might feel pleasant and highly aroused (an affective feeling) on a roller coaster, and your conceptualization of that affect in that context would be "excitement" (an emotional feeling).  In this sense, emotions are what we would traditionally consider to be "cognitive."

Source

Under this scheme, intuition doesn't really have a direct, formal relationship to affect or emotion, although intuitions are often affective (well, pretty much everything is affective).  But see here for a more informed discussion of the literature.


Does teaching a bird an artificial task like eating from a feeder hurt its performance in the wild? Can training a wild animal through operant conditioning somehow cause the animal to forget or be unable to perform tasks which it had perviously learned?

Is it likely that training wild animals through operant conditioning would somehow cause them to be unable to learn or retain other skills? Or is that not how learning actually works?

Does teaching a bird an artificial task like eating from a feeder hurt its performance in the wild?

I wouldn't worry about "running out" of room in our brain. We often forget things just because we don't need to know them, similar to . There are plenty of human savants that display apparently "unlimited" capacities of certain forms of memory, such as Hyperthymesia where one has a seemingly perfect amount of recall of autobiographical details (not to be confused with the largely debunked notion of "photographic memory").

It appears we forget things not because we're low on space, but because we don't need that information (not that there's intent, it's just practical). Information often accessed is strengthened, information never used is weakened and lost. Similarly we physically prune neurons and connections we no longer use in Synaptic Pruning.

Back to the issue of survivability; it's possible that operant conditioning a wild animal could cause them to incorrectly react to natural stimuli. The biggest risk here would be Generalization of stimuli, like Little Albert becoming (temporarily) afraid of all things white and fluffy instead of just the rat he was conditioned with. If you trained a dog that brown furry things means I should attack and he generalizes this to a bear, it won't end well for the dog of course.

This would generally be less of an issue than you might fear however; an animal will quickly forget the conditioned response due to Extinction provided the Conditioned Stimulus is no longer paired with the Unconditioned Stimulus. Repeated exposure of the CS with no US will eventually extinct the reaction; reinforcement learning goes both ways.

It's even more unlikely that completely artificial conditioning will result in prolonged harm to survivability. This is because if the Conditioned Stimulus is never presented, the conditioned response will simply not be activated. The CS won't even need to be extincted, the animal would likely just forget eventually.

Now the one thing I would worry about is Extinction of natural defense/predatory responses. If an animal has learned through experience to do or avoid doing something and, through domestication/etc they no longer feel the urge to run from predators it will of course impact their survival.

It's impossible to say one way or another really, but I hope that helps you understand what's potentially at work here.


Why does an image seem smaller or larger through a pinhole when viewing with human eye I was chewing gum when I took the Trident gum wrapper and rolled it into an open cylinder with a diameter of about 1.5mm (give or take 0.15mm). When I look through the gum wrapper (I have to put it right up against my eye and position it just right to be able to see all the way through), images seem about 10% smaller (extremely back of the napkin assumption) than without the gum wrapper.

This is hard to measure empirically, so I tried to take a photo showing this effect, but the camera showed no difference between the two (the one through the wrapper is brighter, but I think that's just the iPhone camera trying to adjust to the surrounding dark and thus trivial). Just to confirm, I asked 6 people if they see any differences between viewing items through the gum wrapper and without the gum wrapper, and all of them said that the images through the gum wrapper looked smaller than without the wrapper. [EDIT: Asked 4 more people and 3 of the 4 said the image was 5-10% larger than normal]

[EDIT 2: The images also get larger (smaller for the people who said the image was larger) as the wrapper moves away from the eye and towards the object, eventually reaching true size when the wrapper is at the object.]

The only reason I could think of this happening is based on another observation I made. As I brought the gum wrapper into position, objects seemed to bend as they passed over the wrapper in my vision. The only thing I could think of is that the diameter of the cylinder is small enough that this "bend" doesn't have time to even out, and thus collides with the "bend" on the other side of the wrapper and creates a smaller image. However, this assumes that the distortion is causing images to be smaller when viewed through the wrapper. The "bend" distortion could also just be a byproduct of the actual cause of this phenomenon and just a symptom of the image getting smaller.

Why is this occurring?

EDIT 3: More photos that are more out of focus as recommended for more data

(Originally posted in the physics SE site with an account that I lost)

I suspect this is related to distance perception and size constancy. The retinal size of an object (the actual projection of the object on your retina) decreases with 1/distance. However your visual system is compensating for this effect, which is called size constancy. For example if you put one thumb at arm length (~60cm) in front of you and another at half that distance, they will appear roughly the same size, the farther one a little smaller, while it is actually half the size of the closer one. Similarly when you look at yourself in a mirror, your face seems regular size. Next time your are in front of a mirror with condensation, draw the contour of your face in the condensation. You'll be surprised by how small it actually is. Your visual system uses distance cues to perceptually "rescale" objects so that they appear closer to their real size, and not just the size they have on the retina. This is the basis of illusions such as the corridor illusion or Ames' room.

https://en.wikipedia.org/wiki/Ames_room

To go back to your question, when looking at the keyboard through the wrapper you basically eliminate all distance cues (binocular vision, perspective...). Now in an uncontrolled experiment using uncontrolled stimuli it is a bit hard to predict what will happen perceptually, but you can assume that you'll reduce the amount of perceptual constancy and objects will appear smaller (closer to their retinal size), which seems in agreement with your observations. Why does one of your friend perceive it as larger? A similar phenomenon occurs with prisms. With prisms you artificially increase or decrease vergence angle, a cue for distance perception, while preserving the retinal size of an object. Consequently objects appear larger when you decrease vergence (because an object that would elicit the same retinal size but is farther would actually be bigger), or smaller when increase it. However is small subset of the population report perceiving the opposite effect, and as far as I know no one has provided a good explanation of why.

Picture from: Gibson, J. J. (1966). The senses considered as perceptual systems. pp 315.


Why Bayesian Cognitive Modeling? Recently i read an article on Bayesian Program Synthesis. It says that Bayesian cognitive modelling would help AI systems to learn from few examples in comparison to deep learning. But i was not able to understand the advantages of using Bayesian vs other formulations in cognitive modeling. I would like to understand why this Bayesian approach stand out ? What are the drawbacks of current approaches to cognitive modeling ?

Here's a quick answer from general background knowledge, not from any specific knowledge of "Bayesian Program Synthesis (BPS)"

In general, Bayesian models can use strongly informed priors or diffuse "could be anything" priors. Strong priors specify that a lot of parameter values are very unlikely, while a few other parameter values are possible descriptions of the data. With a strong prior, it takes relatively little data to winnow down the possibilities (i.e., faster learning). Weak priors allow for a much broader range of possibilities, but it takes a ton of data to narrow down the possibilities (i.e., slower learning).

Many Bayesian models of mind use strong priors. Such models come pre-set with particular structure or parameter dependencies that are tuned for the type of problem that needs to be learned. This is not "cheating;" the prior is a crucial part of the theory. Another example comes from computer vision: Figuring out what objects and lighting produced a pixelated 2D image can only be done by assuming strong prior knowledge of the types of objects and types of illumination "out there" in the world, otherwise it's an unsolvable problem. An introductory article is here or here (specifically, see the section on "Prior Knowledge" starting on p. 17).

Deep learning, however, is (as far as I know) a generic approach that can learn just about any possible relationship among variables. The cost of this weak prior is that it takes a ton of training to narrow down the parameter distribution.


Can we stop the brain from processing a particular task? Imagine a task of high involvement and great complexity, but one that is not very important, e.g., a strategic computer game. Because of high involvement, the brain continues to process the problem to find solutions after playing the game. Because of the task complexity, I believe there is no right way to solve the problem, and the task is processed by the brain for a very long time but with no solution. The problem is absolutely non-important in 'real life' terms.

Is there a way to "tell" the brain not to process tasks anymore in order to prevent the uncomfortable feeling of having an "unsolved" task?

UPDATE: One of the commentators posted a good additional example of what may happen when your brain continues to process a task:

"A while back I played a game called diplomacy, which is very complex strategically. When I went to sleep that night, thinking about the upcoming turn, my brain was going through all possible combinations of turns and outcomes. One by one. For about 3 hours as I could not fall asleep because of this. While I did find the correct solution, it was quite unpleasant , non normal sleep."

I believe this one is the one of the most unpleasant results of an unwanted task processing. To some extent, a similar thing may happen during the day or even days after the task was "implanted" in the brain. It's just like in a middle of a day, you spontaneously start thinking about that task. So brain was processing that task all the time, it's just you were more busy with other things to not feel it and not start aware thinking of it.

Regarding night time task obsession, I was trying to focus on different things, lying with open eyes, aware thinking of something else, trying to stop the brain, but this doesn't help at all, only makes things worse (because you can't do anything). The solution I found is to not to go to sleep immediately, but to do something different or just rest (do nothing) for approximately an hour, you'll feel after that your brain is calmed a lot. This somehow diminishes that brain task activity and despite, you still may receive task thinking attacks, they won't be so severe, long and pressures.

One answer is through turning off these messages or "tasks" via mindful awareness and focused attention on another task requiring much less cognitive load - like breathing.

Look up Dr. Jeffery Schwartz's book "You Are Not Your Brain" for scientific data on this.

Basically, latest scientific research shows that we can use our mind to stop the brain (or really work around the task, observing it, until it slowly diminishes activity in the bran).

It's the old saying; "mind over matter" - where the brain is also matter.


What is the psychological basis of "survivor's guilt"? Context

I have just been watching a documentary about survivors of the Japanese earthquake and tsunami of March 2011.  Specifically the interviews with ordinary residents of the towns affected.

One thing came through time and again was the notion that was best stated by a friend of mine*- a volunteer firefighter on duty in one of the affected towns on the day of the tsunami:

  what gives me the right to survive, when so many others died?

Question

Obviously, this doesn't just occur in Japan, it seems to happen a lot, where people seem to feel guilty to have survived and feel a sense of responsibility for those who perished.  What is the psychological basis behind this?

Are there any studies that have addressed this?

Side notes

I lived in Japan for 4 years and have many friends from the affected area, this friend of mine was and is still inconsolable that he, in his own mind, could not save more people.

1. Psychological basis of survivor guilt

Psychosocial and evolutionary perspective on survivor guilt

Survivor guilt may be a psychological response that is associated with depression. Loss of a beloved one, which constitutes a psychosocial attachment, can precipitate a proneness towards experiencing survivor guilt. In clinical samples, the clinically depressed tend to suffer from pathogenic cognitions in which they view themselves as harmful to others are an effect of feeling guilty from surviving a beloved one's death (O'Connor et al., 2002). In that regard, we can hypothesise that survivor guilt is probably a self-protective mechanism involving self-denunciation to combat guilt about surviving a beloved one's death.

  Tendency toward self-reproach which death invariably leaves among the
  survivors (Freud, 1987, cited in Ernest Jones, 1960)

Survivor guilt could have evolutionary roots as well: survivor guilt may be a product of evolutionary pressures with living in small groups as a means to promote social organisation (O'Connor et al., 2002). The loss of an individual within these close socially-knit arrangements creates dysfunction and survivor guilt is an evolutionary means to understanding the changes experienced.

Existential crises, anxiety and ambivalence

Drawing from logotherapy, survivor guilt can be understood further from an existential point of view by referring to existential dynamics (Tate et al., 2012):

  Mental health is based on a certain amount of tension [or existential
  dynamics], the tension between what one has already achieved and what
  one still ought to accomplish, or the gap between what one is and what
  one should become. (p. 104)

Survivor guilt may be the tension created between an individual's past experiences and future possibilities. Past experiences such as traumatic events create tension with an individual understanding his or her existence compared to future potentialities. A person narrowly escaping death may physically survive the traumatic experience but in the present moment, they experience excessive amounts of worry about why they are here and what the future holds. This cognitive dichotomy of being shameful about the past and fearful of the future can lead to survivor guilt.

2. Studies on the psychological basis of survivor guilt

Post-traumatic stress disorder (PTSD), cognitive distortions and survivor guilt

Jones and Okulate (2006) conducted a study on the relationship between PTSD and survivor guilt by administering a questionnaire to 1,131 patients from the 68 Nigerian Army Reference Hospital, Lagos, Nigeria. Of these, 194 (22.09%) met the criteria for current
PTSD. Survivor guilt was found in 336 responders (38.26%). The following explanation is given by the authors:

  The
  reason for the very high rate of survivor guilt may be related
  to the intra-group identification and cohesiveness that usually
  develops in combat-effective military units after several years
  of training together. Unfortunately, loss of men resulting from
  death or injury in battle is inevitable. For those who survive,
  witnessing the death of comrades is additional psychosocial
  stressor to the combat situation itself, and the survivor guilt
  that may result is understandably very distressing.

Survivor guilt and chronic illness

Vamos (1997) provides cases on patients and their experiences of survivor guilt in the face of chronic illness and witnessing other people's illnesses:

  Miss A had visited her frequently and  had repeatedly had the
  experience of trying to bright-  en her friend by accounts of shopping
  expeditions or  other excursions, only to feel profoundly guilt-ridden
  that she could still be enjoying herself when her  friend’s life was
  so limited. Since the death, she had  been unable to weep but had
  found herself compelled  to clean both the house and herself
  repeatedly, and  had often wondered whether she should take a  ‘break’
  from dialysis

References

O’Connor, L.E., Berry, J.W., Weiss, J. & Gilbert, P. (2002). Guilt, fear, submission, and empathy in depression. Journal of Affective Disorders, 71(1), 19-27
Tate, K.A., Williams, C. & Harden, D. (2012). Finding purpose in pain: Using logotherapy as a method for addressing survivor guilt in first-generation college students. Journal of College Counselling, 2012, 16(1), 79-92
Okulate, G.T. & Jones, O.B.E. (2006). Post-traumatic stress disorder, survivor guilt and substance use – a study of hospitalised Nigerian army veterans. South African Medical Journal, 96(2), 144-146
Vamos, M. (1997). Survivor guilt and chronic illness. Australian and New Zealand Journal of Psychiatry 1997, 31, 592-596


Freudian repressed unconscious as the biological reason behind self-destructive behavior? Self-destructive habits include:
- smoking whilst being aware of the effects
- not exercising whilst knowing that it is healthier to do so
- taking one more hit of a drug "for the last time, really"

Is there any truth to the following statement?:

Freudian repressed unconscious is what allows us to be in conflict with our emotions. If System 1 were consciously aware of these hidden things, self-destructive behavior wouldn't exist.

This question is inspired by the following book:
O'Connor, Richard - Rewire: Change Your Brain to Break Bad Habits, Overcome Addictions, Conquer Self-Destructive Behavior - Penguin Group US.

It has been a while, but I've always understood the theory to say that the superego, the internalization of values and rules, can cause us to repress ideas that aren't inline with our values. Basically, as we continue to do things that we 'know' are 'wrong' there is a resultant feeling of anxiety, which we often seek to avoid.

There are better ways to explain this type of phenomenon though; I would suggest some basic cognitive behaviourism. For instance, if we suggest that a person's thoughts of guilt, let's say around exercise, create a punishing effect, then we can in turn come to associate exercise with the negative feeling of guilt. If we expand out and include the further associations of obesity/guilt and their close association with exercise, we can start to build a theoretical model of why neurotic behaviors develop around exercise.

-edit-

I'll do a quick edit to respond to the a comment about sources. I was doing some research after I posted this, I managed to find an article discussing how attitudes relate to the avoidance of exercise:

http://onlinelibrary.wiley.com/doi/10.1038/oby.2010.234/full

I'm having a harder time finding anything specifically talking about exercise and the types of avoidance/escape you see in high anxiety behaviour. Here's an article talking about how avoidance and escape can serve as reinforcing mechanism for phobias:

http://www.gracepointwellness.org/1-anxiety-disorders/article/38494-operant-conditioning-and-avoidance-learning


Are there neurological conditions that can be worsened by B group vitamins? I know that vitamins B6 and B12 are very important for the brain function, and both are involved in metabolism of homocysteine. Buildup of homocysteine has been associated with cognitive impairment. There may be dozens of other metabolic pathways that use these vitamins.

I'm interested if there are any medical/psychiatric conditions for which B vitamin supplementation is actually harmful or not advised? could such supplementation overload/deplete the intrinsic factors for these vitamins, making them temporarily unavailable to the brain?

People often fall under the spell of the "more is better" assumption when it comes to supplements, but, while B6 (pyridoxine) has many lifesaving applications (e.g., treating a specific type of seizure, or [protecting the system from acute neurotoxicity of chemotherapeutic agents, B6 can be downright toxic in high concentrations.

Patients with abnormally elevated B6 levels were found to experience numbness and burning pain among other symptoms.  A patient who ingested on the order of 10 grams per day over the long term was found to have muscle weakness and motor deficits in addition to sensory neuropathy.

The most famous anecdote of this was in Oliver Sacks "The Man Who Mistook His Wife for a Hat" under the story entitled "The Disembodied Lady", where a prolonged megadose of B6 left a woman with no proprioceptive feedback about her body in space.  Certainly, there is little or no data about her actual ingested amounts in the popular press account, but this effect was seen frequently as a result of bodybuilding fads in the 1970s and 1980s.

So, the very act of taking the supplement in excess can exacerbate an existing neuropathic condition, or potentially create a pathology where none was present beforehand.

B12 (often supplemented as cyanocobalamin) is a bit of a different animal.  It requires a cofactor ("intrinsic factor") to be absorbed properly, so it's more difficult to inadvertently take in excess.