Why is the order of white/grey matter different in the brain and spinal cord? In the brain proper, grey matter forms the outer layer of the brain, and white matter forms the inner layer. In the spine, this is reversed: white matter forms the outer layer of the spine, and grey matter the inner layer. Is there a developmental or functional reason for this?

I'll tackle this question from a functional point of view.

Gray matter are cell bodies, white matter are myelinated fiber tracts.

In the brain, the gray matter is basically the cortex, the white matter lies mainly underneath it. The Cortex is the place where all the higher mental processing takes place (Fig. 1).

Fig. 1. Cortical functions. Source: Penn Medicine

The white matter in the brain connects the various parts of the cortex so that information can be transported for further processing and integrated.

Fig. 2. Central white matter. Source: NIH Medline

Since the cortex is the 'processor', it makes sense to connect the parts subcortically (more efficient as it leads to shorter connections). However, the cortex has been expanding very late in evolution, so this 'endpoint reasoning' can be contested, because from an evolutionary perspective, more cortex was needed and hence it was expanded right where it happened to be, namely in the outer part of the brain.

In the spinal chord things are pretty much reversed; grey matter within, white matter around it (Fig. 3).

Fig. 3. Section through spinal chord with central grey matter and surrounding white matter. Source: University of Michigan

The white matter, again, is formed by various tracts (Fig. 4) and the grey matter with parts that are processing information (fig. 5).

Fig. 4. Section through spinal chord showing the spinal tracts forming the white matter. Source: Biology.SE

 Fig. 5. Section through spinal chord showing the spinal reflex arches forming the gray matter. Source: APSU Biology

The white matter in the spinal chord constitutes the various sensory and motor pathways to and from the brain, respectively. The gray matter constitutes basic processing nuclei that form the reflex arches in the spinal chord. These reflex arches process incoming sensory information (e.g. pain) and govern motor output (e.g., pulling the hand away from the fire).

Again, the structure makes sense in terms of efficiency, as the reflex arches combine the sensory and motor tracts to govern reflexes, and therefore processing them from within saves space.


What causes fear of failure to lead to lack of effort and actual failure? Background: I'm having hard time motivating myself to study. In my first year I was a very good student, I had the motivation to study because I wanted to compete, it was first and maybe hardest year. I wanted to show that I am good and better. I passed my exams in time with good grades. Then, I started studying less and less, finding it hard to motivate and focus on learning.  I don't study and don't have motivation to study because I am afraid of failing an exam. I am afraid that if I study hard for an exam and then fail I will feel that I am stupid.

Questions

Is there a name for the phenomena of not putting effort into study because of fear of failure which in turn results in actual failure?
What causes this?
Are there any strategies for overcoming this cycle?

Is there a name for the phenomena of not putting effort into study because of fear of failure which in turn results in actual failure?

Yes, this is called self-handicapping.

  Self-handicapping is the process by which people avoid effort in the hopes of keeping potential failure from hurting self-esteem.

  What causes this?

The main and most relevant reason here is the preservation of your own self-image and/or managing your public image. If you were to try your very best and still fail, then the only causal attribution would have been dispositional, that is, the only way to explain it to yourself would have been that, you are just not good enough.

However, when you place impediments in your path and essentially prevent yourself from performing to your fullest, you are creating scapegoats for your failures. This will allow you to attribute the failure to situational factors and not dispositional ones, allowing you to maintain your image of self-competence and/or self-efficacy.

  Are there any strategies for overcoming this cycle?

Self-handicapping occurs in many different fashions but most of them tend to be variations of procrastination and lack of effort/practise. So, by tackling either of these, you will be able to reduce the chances of handicapping yourself.

Other than that, research has shown that by focussing on long-term mastery in a field that you like, self-handicapping behavior can be reduced.

  In three studies with German high-school and college students, we found empirical evidence for the assumed moderator effect of mastery goals. In studies 1 and 3, performance-avoidance goals were remarkably lower associated with self-handicapping in the group of students highly endorsing mastery goals compared to students who proved to be less mastery oriented. In studies 2 and 3, moreover, individuals' self-esteem was less related to self-handicapping when students strongly emphasized mastery goals.


How do some traumatic experiences establish deep beliefs and ideas? Disclaimer - My terminology might be wrong.

How do some memorable experiences that are traumatic or tough, make the brain form some values. Is there a way to establish core values so strongly ourselves through any manual methods? (without needing to go through traumatic experiences)

Childhood experiences have a greater impact than events later on. It is cognitive structure forming time, with a still strong biological background. Also, the child might see itself as vulnerable, thus willing to form bonds with any protective thing that might appear (Giller, 1999):

Chronic early trauma — starting when the individual’s personality is forming — shapes a child’s (and later adult’s) perceptions and beliefs about everything.
Severe trauma can have a major impact on the course of life. Childhood trauma can cause the disruption of basic developmental tasks. The developmental tasks being learned at the time the trauma happens can help determine what the impact will be.

Children can recover to leading normal lives after traumatic events, but not all of them. It gets worst if there are continuous traumatic events (Giller, 1999):

Although most return to baseline functioning, a substantial minority of children develop severe acute or ongoing psychological symptoms (including PTSD symptoms) that bother them, interfere with their daily functioning, and warrant clinical attention. Some of these reactions can be quite severe and chronic.

We go with defense mechanisms to protect ourselves. They might get repressed in our memories but never really fade-out. It is not consensual that it is OK to break down these defenses and make people revive those traumatic experiences. Thus, i do believe you are in a psychodynamic therapy or others. And no, it is not the only way to "reprogram" the brain. There is also cognitive , behavioral, and cognitive-behavioral therapy, which are problem focused, making you relearn the correct way to think/behave in problematic contexts.

CBT for trauma includes: learning how to cope with anxiety and negative thoughts, managing anger, preparing for stress reactions, handling future trauma symptoms, addressing urges to 'self-soothe' with alcohol or drugs and communicating and relating effectively with people (National Centre for PTSD, 2008).
The CBT model when used with survivors of child abuse usually focuses on the 'here and now' rather than revisiting the trauma itself (Henderson, 2006).
Cognitive–behavioral therapy (CBT) techniques have been shown to be effective in treating children and adolescents who have persistent trauma reactions. CBT has been demonstrated to reduce serious trauma reactions, such as PTSD, other anxiety and depressive symptoms, and behavioral problems. Most evidence-based, trauma-focused treatments include opportunities for the child to review the trauma in a safe, secure environment under the guidance of a specially trained mental health professional. CBT and other trauma-focused techniques can help children with cognitive distortions related to the trauma, such as self-blame, develop more adaptive understanding and perceptions of the trauma.

I'd hint that in a context which triggers some childhood trauma (even if it is in a deep layered reasoning), it still keeps that memory being fed, forbidding its physical memory-disposal. Learning the correct reasoning will make these memories fade away eventually.


What is subvocalization good for? While reading, I tend to subvocalize what I have read. I feel this as disturbing, but as many people do this, there must be a reason why the brain does this. So, what is subvocalization good for?

It should be pointed out that subvocalisation while reading is not necessarily of the same cause or purpose as subvocalisation while doing other activities. Many people are able (or accustomed) to comprehending written language only by converting it to spoken language mentally. This allows the interpretation process to share the same brain regions, as opposed to using one modality for reading and another for listening. Naturally some people are more prone to logical (read: serialised) thinking while others are more prone to visual (read: parallel) thinking. Those individuals prone to logical thinking are more likely to subvocalise while reading since this allows the reading process to correspond well with one's usual way of thinking. The reverse should be true for those accustomed to visual thinking.

The act of subvocalising while doing non-reading activities is probably similar in that it may allow the thinking to be of one's usual modality (logical). Taking it further, however, subvocalisation is a way of putting thoughts into words. It is common knowledge that when you put an understanding into your own words you are more likely to develop a lasting memory. This is presumably because explaining something in words requires that the ideas be organised in a coherent fashion, as opposed to possessing merely a superficial glimpse of awareness. To think about it another way, putting thoughts into words creates durable mental objects that can then be stored away into memory.


Batch converting .img files to .mgz in FreeSurfer I have a series of .img files from a previous analysis in SPM that Freesurfer (FS) cannot directly handle.

FS comes with a conversion tool, the mri_convert command, but I am not able to make it run iteratively over all the files in the same directory. I found a mention about the --sdcmlist argument online, however I am not figuring out the proper syntax for it.

When I run:

mri_convert --sdcmlist 000123_1_4.img 000123_1_4.mgz

I get:

mri_convert: missing output volume name

Would anyone suggest a way of going about these conversions?

I couldn't find a way of doing that using the arguments in the mri_convert, so I decided to do it programatically in bash. This answer will only work in Linux (or in any bash). It's an one-line command to iterativelly run the convertion on all files in the same directory.

for f in *.img; do mri_convert $f $f.mgz; done

There is one aspect that I did not get right, that is FS actually handles img files, however these files do not have directionality information, thus using them is not recommended.

One can simply feed the recon-all command with the img file and the command will take care of the conversion.


Can the mind be trained to equanimously observe compulsive urges/cravings (without giving in / acting out)? Are there any practices or habits that one can employ, either frequently or on a daily basis, to train one's mind to equanimously observe (be aware of) compulsive urges or cravings, without giving in to them / acting them out?
Can this skill be developed in a general sense, applicable to all types of urges/cravings, or does one need to train a different, tailored technique to handle each type of urge/craving individually?

According to the article "Brief meditation training induces smoking reduction" one kind of mediation-training reduced smoking by 60% while a control group (relaxation training) showed no such effect.

"Integrative body-mind training (IBMT) is a form of mindfulness meditation that involves body relaxation, mental imagery, and mindfulness training accompanied by selected music background. Cooperation between the body and the mind is emphasized in facilitating and achieving a meditative state. The trainees concentrated on achieving a balanced state of body and mind guided by an IBMT coach and a compact disc. The method stresses no effort to control thoughts but, instead, a state of restful alertness that allows a high degree of awareness of body, mind, and environment."

Other relevant references:
Tang YY, et al. (2007) Short-term meditation training improves attention and self-regulation. Proc Natl Acad Sci USA 104(43):17152–17156.

Tang YY, et al. (2009) Central and autonomic nervous system interaction is altered by short-term meditation. Proc Natl Acad Sci USA 106(22):8865–8870.

Tang YY, et al. (2010) Short-term meditation induces white matter changes in the anterior cingulate. Proc Natl Acad Sci USA 107(35):15649–15652.

Tang YY, Lu Q, Fan M, Yang Y, Posner MI (2012) Mechanisms of white matter changes induced by meditation. Proc Natl Acad Sci USA 109(26):10570–10574.

Tang YY (2009) Exploring the Brain, Optimizing the Life (Science Press, Beijing).


Name this phenomenon: You're shy of doing X because nobody else around you does it I'm looking for the name of the following phenomenon.

Image this situation:

A teenager is riding a bus. He's thirsty. He has a water bottle in his bag, but he doesn't feel comfortable bringing it out and drinking because "I'll look dumb". (Let's assume nobody else in the bus is drinking.)

(I'd also like to know: (1) Are teenagers more susceptible to this?
(2) Does it have to do with self-esteem?)

I think the term you are looking for is social norm, peer norm, or social expectation.

Distinguish from peer pressure, which is a different phenomena, yet related.

Many researchers have shown that teens are more susceptible to peer pressure (which implies the same for peer norms).

Both relate to self-esteem, and while mostly mentioned as facilitators, there is research out there to show that people with low self-esteem are more susceptible to both.

See, for example:

Sumter, S.R., Bokhorst, C.L., Steinberg, L. and Westenberg, P.M., 2009. The developmental pattern of resistance to peer influence in adolescence: Will the teenager ever be able to resist?. Journal of adolescence, 32(4), pp.1009-1021.
Zimmerman, M.A., Copeland, L.A., Shope, J.T. and Dielman, T.E., 1997. A longitudinal study of self-esteem: Implications for adolescent development. Journal of youth and Adolescence, 26(2), pp.117-141.


What do the weights of an artificial neural network represent in biological neurons? In artificial neural networks the connections between neurons are a assigned numbers called "weights" or "parameters". As new data is fed into the neural net, these weights change. This is how the neural net "learns".

I'm trying to understand what these weights might correspond to in a real  brain. The idea occurred to me that it might represent the strength of the myelination on the connections between real neurons.

Is this a correct understanding?

Does the degree of myelineation along an axon vary over time as the neural net processes more experiences?

The weights in an artificial neural network are an approximation of multiple processes combined that take place in biological neurons. Myelination plays a role, but not a major one. Weights in artificial neural networks can be positive or negative numbers.

Weight magnitude. The magnitude of a weight is analogous to a combination of increased dendritic connections between neurons, number of synapses between their dendrites, density of neurotransmitter receptors on the post-synaptic terminals, as well as increased neurotransmitter vesicle formation and fusion on the pre-synaptic terminals.

Positive weights. Positive weights are analogous to the pre-synaptic terminals of the synapses releasing excitatory neurotransmitters (i.e. glutamate). They make it more likely the receiving cell will fire an action potential.

Negative weights. Negative weights are analogous to inhibitory neurotransmitters (i.e. GABA) being released at the synapse. They make it less likely the receiving cell will fire an action potential.

Myelination

Myelination increases the distance that action potentials can travel down the axon. The membrane voltage potential decays much closer to the cell body if the axon is not myelinated. One analogy is that of a garden hose. If the axon is not myelinated, then the garden hose is leaky with holes, and less water pressure (that caries water pressure waves, the action potentials) makes it to the end of the hose.

However, increased myelination is not necessarily analogous to an increased weight. For example, if there are few dendrites between two neurons, with few synaptic connections, then myelination would have little effect.

Learning

You also mentioned learning. During learning, the weights in an artificial neuron increase or decrease. In biological neurons, learning takes place at multiple scales and areas (i.e. non-synaptic and synaptic). At first, during increasing connection strength, you may see increased vesicle fusion, then increased neurotransmitter receptors, then new synaptic boutons, and new dendrites. When "unlearning", or forgetting, these processes happen in reverse.

Overall, a weight in artificial neurons clump a lot of biological complexity into one number that only crudely approximates the degree of connection strength between two biological neurons.


Should you completely get rid of your temptations or do them in moderate amount? So, I am preparing for this really important exam that requires me to give maximum time to studying and lately, I have found myself addicted to this television series. Although I study during my study time very sincerely, I have begun to realize that watching that television series eats a good amount of time in my daily schedule.

I don't know if I should completely cut it out of my schedule, which according to me might make me crave for it even more or I should watch it only in specified time of the day. If I do the latter, I am afraid, I might lose concentration because those scenes sometimes just keeping running in my head, and also I might just end up watching it for longer than I should.

What should I do? Will cutting it out completely make me crave for it even more? Or is specifying a time for it a good idea? What does psychology say?

The problem you are experiencing is called procrastination. You get suddenly very interested in TV shows as a way to avoid the task which is currently generating anxiety.

The relation between a goal (here succeeding in this important exam) and procrastination is well documented (e.g. Bandalos et al. , 2003, in the context of statistics courses). There are two types of goal one can have: Achievement goal (desiring to succeed on an exam, for example) and mastery goal (wishing to understand the content of the course). Sadly, only the first one generates anxiety. Many research found that a desire to understand, not necessarily to succeed, diminishes the procrastination behavior. When procrastination is absent, it also makes us immune to anxiety. Finally, anxiety, when present, tends to produce weaker grades.

(in technical terms: performance goals is positively correlated with procrastination; procrastination is positively correlated with anxiety; anxiety is negatively correlated with the grade obtained; however, mastery goal is negatively correlated with procrastination).

One solution is to set study times, have a schedule for study and a schedule for TV watching, and stick to it. When it is time to study, do nothing else. At first, it will be hard, but in the long run, you will adopt the right automatisms, and study will become easy. Be realistic when setting study times. For example, avoid long study period that are unrealistic. Better have many short periods of two hours and stick to it, rather than a few periods of many hours that are not humanly realistic.

So to answer your question: Your second option is the correct one: determine time slots for study; outside of those times, watch TV if you wish. Your explanation was not correct: it is not craving which makes you watch TV, it is anxiety.

Bandalos, D. L., Finney, S. J., & Geske, J. A. (2003). A model of statistics performance based on achievement goal theory. Journal of Educational Psychology, 95(3), 604-616. doi:10.1037/0022-0663.95.3.604


What is a good beginner's book to read to get a greater understanding of neuroscience? Having read "the mind that changes itself," i've become interested in neuroscience. However reading discussions about this book online there does appear to be controversy about the book and the author doesn't appear to be an actual neuroscientist as well as many scathing reviews online. It still was a good read and factual (i think?). However the actual subject i find very interesting. I was wondering if anyone could suggest a more respected book to give a good introduction, or any good resources to learn from.

You could try this one: 30-Second Brain: The 50 Most Mind-blowing Ideas in Neuroscience, Each Explained in Half a Minute. ISBN-10: 184831647X. I haven't read it myself but it covers a really wide spectrum: single neurons, neural networks, brain architecture, awareness, perception, disease, ageing, etc.
Importantly it's written by really good scientists in who are all currently doing really interesting things.


Is there a region of the brain that mediates pain in a manner reminiscent of the mesolimbic pathway? The mesolimbic dopamine pathway is a common neural pathway upon which rewards converge AKA the pleasure pathway.

So I am trying to find a comparable pathway in the brain for pain -- is there such a thing? Ideally, one where a probe could be inserted and stimulated to induce intractable pain in the victim. Is there anything reminiscent of the mesolimbic pathway but for pain, perhaps with some sort of somatosensory mapping?

What you never thought about using Deep Brain Stimulation to torture someone before?

Based on the most recent (all post-2009) research, it seems to be the same general pathway, just with different gradients in the same areas of the brain. From Taylor et al. (2016):

Recent studies suggest that dopamine neurons in the VTA [ventral tegmental area] and SN [substantia nigra] form a heterogeneous population tuned to either (or both) aversive or rewarding stimuli.
The heterogeneity of dopamine neurons in response to aversive and rewarding stimuli suggests that they serve unique functional roles. Cells activated by reward and inhibited by punishment are well suited to code motivational valence, whereas neurons activated by both rewarding and punishing stimuli are likely to code motivational salience [stimulus awareness]. Neurons coding motivational valence [whether the stimulus is positive or negative in value] would provide a signal for reward seeking, evaluation, and value learning, in line with current theories on the role of dopamine in reward processing. In contrast, neurons coding motivational salience would provide a signal for detection and prediction of highly important events independent of valence, pursuant to dopamine's role in salience processing. These distinct aspects of dopamine neurotransmission might be neuroanatomically separate: dopaminergic neurons coding motivational valence have been found more commonly in the ventromedial SN and lateral VTA with projections to nucleus accumbens [NAc] shell, whereas neurons coding motivational salience are more often reported in the dorsolateral SN with projections to the nucleus accumbens core.

The primary evidence for this updated view seems mostly based (in order of the number of citations) on 3 papers:

Matsumoto and Hikosaka, "Two types of dopamine neuron distinctly convey positive and negative motivational signals", Nature 2009;
Brischoux et al., "Phasic excitation of dopamine neurons in ventral VTA by noxious stimuli", PNAS 2009
Lammel et al., "Projection-specific modulation of dopamine neuron synapses by aversive and rewarding stimuli", Neuron 2011

The part of your question that probably confused Alice and also confuses me a little is that you also ask (in your final paragraph) about somatosensory mapping. The latter doesn't generally involve tracing any pathways beyond the sensory areas of the brain, e.g. for macaques

Also such maps are not totally fixed as there is some use-dependent plasticity.


What is the most comprehensive model of executive control? Wikipedia has a nice summary of the various models of executive function, but what is the most comprehensive one? That is, the one that accounts for the most cognitive variations among subjects and can be applied to the most tasks.

Currently, the most comprehensive cognitive model of executive functions would have to be the model proposed by Miyake et al. (2000).
(It is probably best not to confuse being the most comprehensive cognitive model with being a strong explanation, because the executive functions remain one of the most poorly understood areas of cognition, but it's a very useful model.)
Miyake-Friedman Model

This individual differences study examined the separability of three often postulated executive functions—mental set shifting (“Shifting”), information updating and monitoring (“Updating”), and inhibition of prepotent responses (“Inhibition”)—and their roles in complex “frontal lobe” or “executive” tasks.

This influential model has engendered thousands of papers applying it to explain many different findings and domains. Psychometric research using confirmatory factor analysis (Duan, Wei, Wang and Shi, 2010) found support for three shifting, updating and inhibition factors, and Friedman et al. (2006) reported evidence for the factors' discriminant validity by comparing it with the Wechsler IQ scale. Practical support for the model has also come from research on ADHD, as reviewed in Wilcutt et al. (2005), and attentional problems in school settings (Friedman et al., 2007).
Finally, the NIH Toolbox Cognition Battery also includes an executive functions test informed by the Miyake and Friedman model, which recently received strong support in a review by Zelazo et al. (2013):

In the current study, we sought to assess the reliability and validity of new measures of EF and attention that are part of the NIH Toolbox CB. New versions of the DCCS and the flanker task were designed to provide assessments of two aspects of EF, cognitive flexibility (Toolbox DCCS) and inhibitory control in the context of visual selective attention (Toolbox Flanker). Together with a separate measure of working memory (see Tulsky et al., Chapter 5, this volume), these measures capture the three aspects of EF identified by Miyake et al. (2000) in their work with adults.
Overall, results reveal excellent developmental sensitivity across childhood, excellent test–retest reliability, and excellent convergent validity (except for the Toolbox Flanker, which showed adequate convergent validity among 8–15 year olds). Correlations between the new NIH Toolbox measures and corresponding convergent measures were generally quite high, although for younger children, they were higher for the DCCS than for the flanker measures.

Overall, the tripartite Miyake and Friedman model is extremely well-supported by both the literature and praxis. If a more comprehensive cognitive model of executive function exists, I am not aware of it.
References

Duan, X., Wei, S., Wang, G., & Shi, J. (2010). The relationship between executive functions and intelligence on 11-to 12-year-old children. Psychological Test and Assessment Modeling, 52(4), 419-431.
Friedman, N. P., Haberstick, B. C., Willcutt, E. G., Miyake, A., Young, S. E., Corley, R. P., & Hewitt, J. K. (2007). Greater attention problems during childhood predict poorer executive functioning in late adolescence. Psychological Science, 18(10), 893-900.
Miyake, A., Friedman, N. P., Emerson, M. J., Witzki, A. H., Howerter, A., & Wager, T. D. (2000). The unity and diversity of executive functions and their contributions to complex “frontal lobe” tasks: A latent variable analysis. Cognitive psychology, 41(1), 49-100.
Willcutt, E. G., Doyle, A. E., Nigg, J. T., Faraone, S. V., & Pennington, B. F. (2005). Validity of the executive function theory of attention-deficit/hyperactivity disorder: a meta-analytic review. Biological psychiatry, 57(11), 1336-1346.
Zelazo, P. D., Anderson, J. E., Richler, J., Wallner‐Allen, K., Beaumont, J. L., & Weintraub, S. (2013). II. NIH toolbox cognition battery (CB): measuring executive function and attention. Monographs of the Society for Research in Child Development, 78(4), 16-33.


Can brain zaps be demonstrated by EEG? Brain zaps are explained as an electrical buzz in the head and the symptoms occur while withdrawing slowly from an SSRI antidepressant medication.

Is it possible to detect brain zaps by placing EEG electrodes on the locations where many people report the phenomenon to occur (neck, spine, arms, ears, eyes, lips)?

Short answer
I haven't been able to find studies on EEG correlates of antidepressant discontinuation syndrome.

Background
'Brain zap' is a colloquial term for antidepressant discontinuation syndrome.

Note that the sensations you mention in the arms, neck and lips etc are likely caused by central effects (i.e., in the brain) that evoke sensory perceptions as if they occur peripherally. Hence, any electrical activity associated with antidepressant discontinuation syndrome should, likely, be sought in the cortex.

I did a literature search on Antidepressant discontinuation syndrome AND EEG and I couldn't find anything.

The EEG is classically used to detect gross disturbances in the brain, like epileptic activity. Epileptic discharges are paroxysmal events characterized by large parts of the cortex being synchronously entrained in activation. Because it is the cortex that is activated, the EEG electrodes are right on top of where the activity is and hence pick it up easily. Furthermore, the amplitude of epileptic EEG activity is very high compared to the normal background EEG (Fig. 1), because large parts of the cortex fire synchronously. The clinical symptomatology of epilepsy is hence expressed as gross changes in motor behavior (convulsions), loss of consciousness or other signs (Smith, 2005).

Those brain zaps are comparatively benign events:

  Most cases of discontinuation syndrome last between one and four weeks, are relatively mild, and resolve on their own...

(source: wikipedia)

Hence these 'zaps' may not pop out so easily above the background EEG. Further, epileptic discharges happen often, even in the absence of clinical symptomatologies, so they are picked up easily. Moreover, epileptic activity can often be provoked, for example by flashing a stroboscope in fron of the sufferer. Evoked activity can more easily be registered with EEG because the time window of interest is defined. Brain zaps on the other hand may be less common and the electrophysiologist would simply have to wait for them to occur. And even then, mild brain activity may not be sufficiently different from background EEG to yield a proper signal.

Fig. 1. EEG of epileptic discharges show up clearly against the background EEG. source: Smith (2005)

Reference
- Smith, J Neurol Neurosurg Psychiatry (2005); 76(SII): ii2–7


How to measure change in emotional responses when pre and post tests use different measures? My research is to evaluate change of emotional responses of participants, after performing two types of game activities. Two groups of participants, Group A and Group B, will be assigned to Activity A and Activity B respectively. The research design does not cater for a control group.

I plan to measure the baseline emotions (using the Mood Questionnaire) [1] of all the participants. The arousal and valence components will be measured using the Self Assessment Manikin (SAM) questionnaire [2]

So now, I have pre-test responses from Mood Questionnaire (baseline emotional responses), and the post-test responses from SAM.

I am not sure how to proceed with the data from each instrument. For instance, how do I obtain a change in emotional responses from each subject? How do we normalize the baseline emotions in this case?

Mood Questionnaire available at
[1] https://www.metheval.uni-jena.de/mdbf.php

SAM questionnaire available at
[2] http://irtel.uni-mannheim.de/pxlab/demos/index_SAM.html

Normally, I'd recommend using the same mood measure pre and post manipulation. This allows you to assess the size and direction of change. It also likely removes more error variance from the post-test measure (which would increase statistical power), because using the same measure is likely to increase the correlation between pre and post.

That said, if you've used different measures pre and post, then you could perform an ANCOVA with group as independent variable, baseline mood as the covariate, and post-test mood as the dependent variable.

A slight possibility is that you could  map scores on both tests to a common scale. This might allow you to make qualified claims about whether emotions increased or decreased. That said, this would require that you have access to additional data on people who completed both tests in a non-experimental context. You could then use the means and correlations between the two tests to develop a mapping to a common scale.


How does Cannabis cause psychosis? Whenever I research cannabis induced psychosis, I mostly get two types of results:

1) Cannabis causes psychosis directly and a bunch of other issues (mostly misleading propaganda)

2) There is no evidence that cannabis actually causes psychosis directly, rather it seems to be a correlation issue. (also misleading propaganda)

However, my two best friends experienced permanent psychosis immediately after a heavy cannabis use episode (on separate occasions).

I am convinced that cannabis is perfectly capable of causing or "unlocking" psychosis. I don't think that there is any question to this.

But how does it actually work?

In one of the cases, my friend had some very strong cannabis to smoke, after which he started to hear voices, and this never ended, even months after stopping smoking. Only after anti psychotic medication (Seroquel) did the symptoms stop, and they seem to be permanent, stopping the medication causes the symptoms to come back.

From what I understand, Seroquel suppresses dopamine, while cannabis has nothing to do with dopamine.

So how does cannabis induce a dopamine related disorder?

Research into the "how" is ongoing. From the most recent review I could find, the effect of cannabis on the dopamine system is not entirely elucidated, even on a quantitative level:

  The onset of effects of THC appears to be delayed relative to the onset
  of other psychotomimetic drugs, suggesting that the effects of THC may be downstream to its
  primary site of action. Given that the endocannabinoid system is principally a neuromodulatory
  system, perhaps the psychosis-relevant effects of THC are related to the consequences of CB1R
  activation on other neurotransmitter systems implicated in the neurobiology of psychosis.
  Cannabinoid Dopaminergic Interactions: Single doses of dopamine (D2) receptor antagonists
  (olanzapine and haloperidol) have been shown to reverse the acute psychotomimetic effects of
  THC in healthy subjects in two HLS (5, 6) although not in the third (7). Furthermore, chronic D2
  antagonist treatment failed to protect schizophrenia patients from the symptom exacerbating
  effects of THC (32).

  Preclinical studies demonstrate that THC administration increases striatal dopamine
  release by 25-100%, but the human data are mixed with two studies reporting no significant
  increase (91, 92) and one study reporting a 3.9% increase in striatal dopamine release (93).
  These studies had small sample sizes and differed in the THC doses, routes of administration
  and imaging methodology. A re-analysis combining data from two studies (91, 93) reported a
  significant but small increase in THC-induced dopamine release (94). Of note, in contrast to
  amphetamine and cocaine, which induce large increases in striatal DA release (10-30%) in
  humans, THC at doses that produce robust behavioral effects induces small (2-5%) increases in
  dopamine release. More recently, Kuepper et al, 2013 reported that individuals with psychosis as
  well as those with a family history of psychosis demonstrated THC-induced striatal dopamine
  release, but this was not observed in the controls suggesting that dopamine may be involved
  particularly in the effects of THC in those with an increased risk for psychosis (95).

The review also covers several genes that have been implicated in both schizophrenia and vulnerability to THC-induced psychosis:

  In the striatum, clearance of synaptic dopamine is highly dependent on the dopamine
  transporter (DAT). A polymorphism of the DAT1 gene is associated with lower enzymatic activity
  and thus, higher dopamine levels in the striatum, and has previously been associated with
  schizophrenia (81). Bhattacharyya et al. reported that individuals with the 9-repeat allele showed
  increased sensitivity to acute THC-induced psychotic symptoms (82).

  The enzyme AKT1 inactivates glycogen synthase kinase by phosphorylation and their
  interaction has been implicated in schizophrenia (83, 84). Cannabinoids stimulate the AKT1
  pathway via CB1Rs and CB2Rs. Bhattacharyya et al found that a polymorphism of the AKT1
  gene (the GG genotype of the SNP rs1130233) moderated sensitivity to the acute psychosisinducing
  effect of THC (82). Furthermore, a synergistic influence of DAT1 and AKT1 genotypes
  on THC-induced psychotomimetic effects was also reported.

All the DAT/AKT1 data on healthy individual using cannabis with is based on exactly one study, so I reproduce their graphical finding below:

Alas they only reported total PANSS.

In the review, there's more discussion of COMT, which has seen more attention, but suffice to say the results on that have been mixed. It remains to be seen in  the DAT1/AKT1 study can be replicated. It does seem that AKT1 alone has an impact, based on more studies that found the same polymorphism of AKT1 impacts first-episode psychosis in cannabis users and psychotomimetic effects in healty cannabis smokers.

I find it interesting that yet another study on first-episode psychosis has implicated AKT1 polymorphism, however, this time with an interaction that enhanced its effect... except that the other gene involved was not DAT1 (as in the case of psychotomimetic effects on healthy individuals) but rather with DRD2.

Perhaps 10 years from now, this question will have a less tentative answer.

To further complicate the issue, cannabis has more than one active substance:

  CBD is the second most prominent
  cannabinoid in cannabis. Unlike THC, CBD displays CB1R antagonism/inverse agonism
  amongst several other modulatory effects on the endocannabinoid system. The potential
  antipsychotic effects of CBD have drawn increasing attention (20) and some HLS have
  examined the interactive effects of THC and CBD. Pretreatment with CBD is associated with
  lower THC-induced psychotomimetic effects, paranoia and verbal memory impairments (12, 21).
  Furthermore, while THC resulted in increased psychotic symptoms and skin conductance
  responses during processing of fearful faces; CBD, led to a reduction in anxiety and a decrease
  in skin conductance response (22).

For more, there's a slightly older review that's freely available in PMC.

Yet another review that focuses only on THC's effect on dopamine mentions some of the challenges in observing dopamine changes in humans following THC administration: insufficient PET camera resolution and doses that are substantially less than those used in animal models.


What is the result of an excess of dopamine? I'm pretty familiar with the results of having not enough dopamine, though the reasons are not so clear to me.

To get a better insight on the topic I'd like to know something about having too much dopamine:

What behaviour is result of having too much dopamine?
Why does it happen?

I am aiming to get insight in disease states associated with excess dopamine, not drug-induced states.

Too much dopamine release in the striatum may lead to psychosis, and especially to the positive symptoms associated with this disease (e.g., delusions and hallucinations, as opposed to the negative symptoms such as a flattened affect) (Laruelle et al., 1999).

The etiology of psychosis is complex. Many direct and indirect environmental factors are implicated, as well as genetic factors. Environmental factors include obstetric complications and frequent cannabis or amphetamine use. The environmental factors are all implicated stronger in psychosis than genetic causes. Genetic predisposition and environmental factors may also interact in complex ways in the development of psychosis (Howes & Kapur, 2009).

References
- Howes & Kapur, Schizophrenia Bulletin (2009); 35(3): 549–62
- Laruelle et al., Biol Psychiatry (1999); 46:56–72


Can an autistic person have very advance language skills? Can an autistic person have very advanced language skills (Verbal communication, not about tonal nor body language skill, nor the written verbal language, I keep dyslexia out of this discussion for sake of specificity) and a very Early age of first talk, while having other autism symptoms?
Notably there are a few blogs and many social media posts that writes about "hyperverbal autistics" but I did not find scientific literature about hyperverbal autistic people.

They may be referring to hyperlexia (rather than hyperverbal ability):

Hyperlexic children are characterized by word-reading ability well
above what would be expected given their age. ... Some experts believe
that most children with hyperlexia, or perhaps even all of them, lie
on the autism spectrum.

But as far as verbal ability goes, since autism is a spectrum disorder, there is bound to be a spectrum of verbal abilities in those afflicted.  Wikipedia summarizes:

Language impairment is also common in children with autism, but it is
not necessary for the diagnosis. ... It is also common for individuals
with ASD to communicate strong interest in a specific topic, speaking
in lesson-like monologues about their passion instead of enabling
reciprocal communication with whomever they are speaking to.

In other words, "hyperverbal" autistics are hardly unusual.  However, they often struggle with perspective-taking, and hence may speak out of turn, failing to assess their audience's level of interest.
For recent reviews of language acquisition and verbal abilities in individuals with ASD, see for example:
Eigsti et al (2011); "Language acquisition in autism spectrum disorders: A developmental review":

... early studies indicated that some 50% of affected individuals
never acquire functional speech, though more recent estimates find a
smaller proportion of non-verbal individuals, typically around 25%.
Language acquisition in ASD is characterized by dramatic delays, with
first words produced at age 38 months, on average, compared to 8–14
months in TD.

Volkers (2017); "Untangling the Language Challenges of Autism":

... on average, children on the spectrum produce their first word one
to two years later than typically developing children. And we know
that language ability among children on the spectrum varies
greatly—some may be fluent conversationalists, while others can barely
speak.


What is the psychology behind choosing to be weird? There is a saying I was once told:

  "I no longer fear going insane, I am enjoying every moment of it"

For some (including myself), this is in fact a rather happy and liberating reality, albeit a reality that I don't quite understand.  So, my question is, what is the psychology behind choosing to let one's weird side show?

Please note - I am not asking for self help, don't need it - just trying to understand the psychological aspects.  An example of this is when I wore a ballerina suit and walked around a shopping centre as if nothing was out of the ordinary... it was not a pretty sight

The psychology behind choosing to let one's weird side show?
I think the this question would work as effectively as:
The psychology behind choosing to let one's individuality show?

Human beings are social animals. Social pressures  play significant factors in moulding personality.

  The term conformity is often used to indicate an agreement to the
  majority position, brought about either by a desire to ‘fit in’ or be
  liked (normative) or because of a desire to be correct
  (informational), or simply to conform to a social role
  (identification).

So assuming "weird" is more likely to be further away from social norms. The more social pressure to be borne. This means a greater courage is needed to be oneself. There are links between self-acceptance, social pressure and depression.

  Correlational results indicated that all three trait dimensions of
  perfectionism (i.e., self-oriented, other-oriented, and socially
  prescribed perfectionism) were associated negatively with
  unconditional self-acceptance. Also, as expected, depression was
  associated with relatively low unconditional self-acceptance. Finally,
  a path analysis revealed that unconditional self-acceptance mediated
  the association between socially prescribed perfectionism and
  depression, and other-oriented perfectionism was found to affect
  depression only indirectly through its association with low levels of
  self-acceptance.

Dimensions of Perfectionism, Unconditional Self-Acceptance, and Depression
Gordon L. Flett, Avi Besser, Richard A. Davis, Paul L. Hewitt
Journal of Rational-Emotive and Cognitive-Behavior Therapy
June 2003, Volume 21, Issue 2, pp 119-138

Conclusion
Gaining self-acceptance, one's individuality or "weirdness" is inversely proportional to the incidence of depression; and also improves the individual's capacity to cope with social pressure to conform.  So by accepting one's strengths and weaknesses one is freed from (social and psychological) pressure, improving one's sense of well being.


How well can a human-generated "random number" be predicted? For example, if i ask an individual to write a 20-number-long sequence of random numbers from 0 to 10. How well can I predict the 20th number from the initial 19?

More generally,

How well can subsequent numbers in a sequence be predicted from previous numbers?
How well can humans generate random sequences of numbers?

It seems like there is a fairly big literature on this topic.

Wagenaar (1972) provides an early review of research. The author summarises around 15 studies. The studies involved generated random elements including letters and numbers of varying lengths. In all but one study, participants were deemed to be not good at randomising. As part of their review they talk about various forms of nonrandomness and factors that increased the nonrandomness (e.g., naivity of subjects regarding types of randomness, boredom, presence of a natural order to the objects, etc.). In general participants either engaged in too much alternation or too many runs of the same response. Wagenaar (1972) noted the need for more research. The general model seemed to be one whereby stable individual differences (e.g., memory, skill, and mental representations of randomness), states (e.g., boredom, fatigue), and inherent constraints on human randomness generation interacted to influence the degree of randomness produced.

Towse and Neil (1998) provide software call RgCalc for evaluating randomness in human generated sequences.

Brugger (1997) provides a more recent review, summarising:

  It is conjectured that Tune's explanation of sequential nonrandomness
  in terms of a limited capacity of short-term memory can no longer be
  maintained. Rather, interdependence among consecutive choices is
  considered a consequence of an organism's natural susceptibility to
  interference. Random generation is thus a complex action which demands
  complete suppression of any rule-governed behavior.

I also found a couple of articles by Persaud (2005) and Figurska et al (2008) that might be relevant.

Summary: Humans typically display some form of nonrandomness when generating sequences of digits. The degree of this nonrandomness varies across people. It is unclear to me at this point how well individuals could perform, for example, if they had an aptitude for random number generation or were trained to generate random numbers. For example, individuals might be able to draw on cues in the external world that are random and use that as their own personal input for generating responses (but perhaps this would be considered cheating).

However, the nonrandomness may only enable very small incremental prediction above chance in predicting any given response. Furthermore, presumably longer initial sequences of response would improve the ability to guess the subsequent response. Having longer sequences would allow you to extract the form of nonrandomness that the particular individual adopts (e.g., do they prefer alternating numbers or runs, do they prefer some digits over others, are there sequences of numbers preferred).

References

Brugger, P. (1997). Variables that influence the generation of random sequences: An update. Perceptual and Motor Skills, 84(2), 627-661.
Figurska, M., Stańczyk, M., & Kulesza, K. (2008). Humans cannot consciously generate random numbers sequences: Polemic study. Medical hypotheses, 70(1), 182-185.
Persaud, N. (2005). Humans can consciously generate random number sequences: A possible test for artificial intelligence. Medical hypotheses, 65(2), 211-214.
Towse, J. N., & Neil, D. (1998). Analyzing human random generation behavior: A review of methods used and a computer program for describing performance. Behavior Research Methods, Instruments, & Computers, 30(4), 583-591.
Wagenaar, W. A. (1972). Generation of random sequences by human subjects: A critical survey of literature. Psychological Bulletin, 77(1), 65-72.


Cognitive-Behavioral Therapy Limitations In treating people with Cognitive-Behavioral Therapy:

Which people can't be helped by therapy?
How are some people more treatable than others?

Additional Info

In the comments of a blog post analyzing male seducers, a psychotherapist explained the effect of narcissistic mothers on their sons. She said that some people have a greater capacity for benefiting from therapy than others. Some people can't be helped by therapy.

What makes a person unable to benefit from therapy?

I came across this question whilst researching CBT for a course I am studying.

The short answer

As I will cover in the long answer, there has been a lot of articles stating that CBT is very effective, and there are articles which have stated that it is not as effective as has been claimed.

  CBT is not a single model of therapy, applicable to all clients in all situations.  This has been one of the criticisms levelled at CBT, that its 'one size fits all' approach to the complex nature of human problems will, inevitably, fail to meet the needs of many, or (at best), simply focus on symptom reduction. (Reeves, 2013)

There are a fair few factors which can prevent CBT from becoming effective, and a trained and certified CBT practitioner will be able to assess the suitability of CBT.  If they operate ethically, they will not go ahead with providing CBT to someone who it would not benefit.

One of the biggest factors which doesn't allow CBT to work is that if the client is not willing or able to challenge their thoughts and behaviours, then CBT will not be effective.

Long answer

For the long answer, which will help to explain some of the reasons why CBT may not work with some people, I will be using a lot of the work I put into an essay I had to write for my psychotherapy course which covered Cognitive Behavioural Therapy (CBT) and integrative approaches to therapy.

CBT is an integrative model of approach and we had to look at how an integrative approach may be used to support the client within a case study provided.

Case study provided

Hassan has been referred to you for work-related stress and anxiety.  He has a management position and is finding it difficult to cope.  At present the information you have is that he is a 42 years old Muslim man, married with 2 children.  He has lived in the UK since the age of 5 when his parents travelled here.  His father died two years later and Hassan, as the eldest son, has felt responsible for the wellbeing of his mother and sisters as well as his own family.

Your referral is through an employee assistance scheme.  Hassan’s assessment shows high level of anxiety without depression.  He is otherwise fit and healthy.  You may offer him six sessions with a further six sessions if appropriate.

An article (Dhami & Sheikh, 2000) adapted from a chapter in Caring for Muslim Patients, published by Radcliffe Medical Press, Oxford, England; provides key insights needed to allow Muslim clients' concerns to be adequately heard.  The vignettes section of the article gives a few sayings of Muhammad regarding relationships with parents and one of them points out that you should “strive to serve them”.

If the client has had the opportunity to fully integrate with the western culture they are living in, they may be more open to challenging their thoughts and beliefs, however we need to be mindful that as therapists, just like we are not here to judge, for an example, on sexuality (Pink Therapy, 2016) (UKCP, 2015), we are not in a position to judge whether a cultural or religious belief is right or wrong, especially when we are not priests, vicars, rabbis, imams or the like.  Not only that, if the client is devout in their religious beliefs, then we are not going to change those beliefs very easily, if at all. (Babilonia, 2015)

The only time when we can intervene in any religious or cultural beliefs is when it is believed that laws may be broken such as the FGM Act (Home Office, 2016) (Crown Prosecution Service, n.d.), in which case, we would refer the legal case to the necessary authorities and it would be down to the legal profession and not the therapist.

Strengths and Limitations of integrative approaches to counselling

Strengths

Integrative counselling and psychotherapy can be seen as one of the most effective approaches within counselling. (The Counselling Directory, 2013)  The idea behind the integrative approach is that no single approach suits every client and therefore you use different approaches and models of therapy to suit the situation and client.  The article within The Counselling Directory cited also states that integrative therapy has four different categories:

common factorsLooking at the common tools available in each approach that can be useful in the therapy.  Therapist/Client rapport, therapist qualities – positive regard, and congruence etc. – emotional release, and clarification etc.
technical eclecticismThe therapist looks at and selects the best interventions by relying on experience and knowledge of what has worked in the past for others, through theories and research literature.
theoretical integrationThe combination of two approaches with a common philosophy.  The combined ideas are theoretically the same as each other.  For example, cognitive behavioural therapy (CBT) is part of the theoretical integration category, as it is a combination of behaviourism and behaviour therapy, and cognitive theories and their application in therapeutic settings (Reeves, 2013), plus, cognitive analytical therapy is also a theoretical integration of psychodynamic therapy and cognitive therapy.
assimilative integrationThe therapist primarily sticks to one therapeutic approach, for example Humanistic or psychodynamic, but the therapist will use strategies and models from other therapeutic approaches as well.  The combination of ideas will assimilate the pure form of the primary therapeutic approach.

Limitations

The limitations of any integrative therapy depend on the category of integration.

Theoretical integration

One problem identified in theoretical integration is that it is difficult to integrate some theories; for example, it is difficult to integrate psychodynamic theory and behavioural theory.  The psychodynamic approach suggests that our early experiences from birth onwards and their impacts lead to our psychological problems, where behaviour theory sees problems as much more agreeable to change (Reeves, 2013).  These differences result in incompatibilities between these theories.

Assimilative integration

With this kind of integration, there is no balance compared to the other forms of integration.  Where the therapist is primarily psychodynamic or humanistic, for example, they will pick and choose ideas from other approaches which may not be put forward by their primary approach, but can work very effectively and contribute to the treatment or treatment plan.

Technical eclecticism

This shares similarities and differences with assimilative integration, but it has no theoretical underpinning to the approach. (The Counselling Directory, 2013)

As CBT is a theoretical integrative model, and it is difficult to integrate some theories, CBT cannot and does not incorporate any psychodynamic theories.  However, if you are going to work in a fully integrative manner, you need to bear in mind the theories within the psychodynamic approach too.  If therapy seems to need some psychodynamic interventions, then you may need to drop CBT sessions sometimes and concentrate on the psychodynamic interventions, maybe through Cognitive Analytical Therapy instead, before continuing with CBT.

The basic concept of CBT

Cognitive Behavioural Therapy (CBT) was developed by Aaron Temkin Beck, and as mentioned before, CBT is a combination of behaviourism and behaviour therapy, and cognitive theories and their application in therapeutic settings (Reeves, 2013).  CBT helps to change how you think, hence the word Cognitive, and what you do, hence the word Behaviour.

A difficult life situation, relationship or practical problem can lead to:

Altered thinking
Altered emotions and feelings
Altered behaviour
Altered physical feelings or symptoms

Things can happen the other way too.  Any of the above alterations can lead to a difficult life situation, relationship or practical problem (Royal College of Psychiatrists, n.d.).

CBT works by trying to get the client to think about a situation in a more helpful way in order to move forward using more helpful behaviours.

The basic concept of REBT

Rational Emotive Behaviour Therapy (REBT) has generally been put under the same umbrella as CBT, however although it has similarities, REBT is different.  Where CBT was developed by Aaron Beck, REBT was developed by Albert Ellis when he started to lose faith in the type of psychoanalysis he was using.

REBT is a practical and action-led model of therapy and personal growth.  It doesn’t just focus on the client’s behaviours, but also allows the client to understand the behaviours of others and provide techniques that will help to solve future problems.

Although REBT looks primarily at our current beliefs and behaviours, it also looks at the cause and effect of past experiences and beliefs which create our present beliefs and behaviours.  It does this whilst aiming to change irrational beliefs into rational ones quickly rather than slowly, however, one key point to note is that the therapist does not impose rational beliefs on the client, but accepts there are non-rational beliefs that may help people achieve happiness.  That way, the therapist is accepting the client’s value system.

REBT, uses an A-B-C-D-E formula.

Activating ExperienceAlso referred to by some as the Initial Sensitising Event (ISE), this is the root cause of our unhappiness
BeliefsIrrational self-defeating beliefs that are the source of our unhappiness, or come about as a result of the ISE
ConsequencesThe neurotic symptoms and negative feelings and emotions that result from the ISE and/or Beliefs
DisputeWe must dispute and challenge these irrational beliefs in order for the client to enjoy a balanced outlook in life
EffectsThe client must learn to enjoy the effects of the new rational beliefs and get used to the changes, letting them become the new norm.

The shortfalls of CBT

As mentioned before, One of the ideas put forward about CBT is that it is a suitable form of therapy for all human problems.  This idea can be damaging in some respects, as CBT is not suitable for all psychological conditions.

Interestingly, whilst researching the overall efficacy of CBT, I came across a few items of note.

Carl Rogers emphasised the quality of the therapeutic relationship as a necessary and sufficient condition for successful therapy (Rogers, 1957) whereas CBT therapists tend to see the alliance as more instrumental in ensuring the patient’s adherence to the treatment protocol (e.g. Dunn, et al., 2006) (Goldsmith, et al., 2015)
The Countess of Mar in the House of Lords suggested the results of a trial into the effectiveness of CBT and GET (graded exercise therapy) had been artificially inflated (BACP, 2013)
An international team of researchers (Cuijpers, et al., 2016) concludes that

  …CBT is ‘probably effective’ with major depression, general anxiety disorder, panic disorder and social anxiety disorder, but not as effective as has been claimed, due to publication bias, poor quality of studies, and the use of waiting list control groups as a comparator. (BACP, 2016)

CBT is as much based on the development of a therapeutic alliance as it is in a psychodynamic and humanistic approach.  The success of therapy will be, at least partly, informed by the nature of the therapeutic process, and not simply the application of particular theoretical ideas, as some suggest (Reeves, 2013)
Recent literature provides fairly strong evidence that CBT in addition to antipsychotic medication is effective in the management of acute as well as chronic schizophrenia (Rathod & Turkington, 2005).  However, I would stress that CBT was not used alone in any of these studies from what I have seen.  It was used carefully in conjunction with psychiatric help and antipsychotic medication.

An alternative to CBT called Metacognitive Therapy (MCT) has been touted to be better than CBT. But it was developed by Manchester University (Addelman, 2020) and studied by Manchester University (Wells, 2019) so more independent studies are needed.

Either way, if the client is not able or willing to challenge their thoughts and behaviours, then CBT will not be effective.

References

Addelman, M. (2020). New therapy more effective than cognitive behavioral therapy for depression.
Retrieved from: https://medicalxpress.com/news/2020-05-therapy-effective-cognitive-behavioral-depression.html

Babilonia, S. (2015). Challenging religious privilege in public life.
Retrieved from: http://churchandstate.org.uk/2015/10/the-problem-with-faith-11-ways-religion-is-destroying-humanity/

BACP. (2013). Policy. Therapy Today, 24(2), p. 52.

BACP. (2016). News. Therapy Today, 27(8), p. 6.

Crown Prosecution Service. (n.d). Female Genital Mutilation Legal Guidance.
Retrieved from: http://www.cps.gov.uk/legal/d_to_g/female_genital_mutilation/#a02

Cuijpers, P. et al. (2016). How effective are cognitive behavior therapies for major depression and anxiety disorders? A meta-analytic update of the evidence. World Psychiatry, 15(3), pp. 245-258. https://doi.org/10.1002/wps.20346

Dhami, S. & Sheikh, A. (2000). The Muslim family: predciament and promise. The Western Journal of Medicine, 173(5), pp. 352-356. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071164

Dunn, H., Morrison, A. P. & Bentall, R. P.  (2006). The relationship between patient suitability, therapeutic alliance, homework compliance and outcome in cognitive therapy for psychosis. Clinical Psychology & Psychotherapy, 13(3), pp. 145-152. https://doi.org/10.1002/cpp.481

Goldsmith, L. P., Lewis, S. W., Dunn, G. & Bentall, R. P. (2015). Psychological treatments for early psychosis can be beneficial or harmful, depending on the therapeutic alliance: an instrumental variable analysis. Psychological Medicine, 45(11), pp. 2365-2373. https://doi.org/10.1017/S003329171500032X

Home Office. (2016). Mandatory reporting of female genital mutilation: procedural information.
Retrieved from: https://www.gov.uk/government/publications/mandatory-reporting-of-female-genital-mutilation-procedural-information

Pink Therapy. (2016). Why I am resigning from the British Association for Counselling and Psychotherapy. Retrieved from: https://pinktherapyblog.com/2016/02/17/why-i-am-resigning-from-the-british-association-for-counselling-and-psychotherapy/

Rathod, S. & Turkington, D. (2005). Cognitive behaviour therapy for schizophrenia: a review. Current Opinion in Psychiatry, 18(2), pp. 159-163. https://doi.org/10.1097/00001504-200503000-00009

Reeves, A. (2013). An Introduction to Counselling and Psychotherapy: From Theory to Practice. London: SAGE Publications Ltd..

Rogers, C. (1957). The Necessary and Sufficient Conditions of Therapeutic Personality Change.
Retrieved from: http://www.shoreline.edu/dchris/psych236/Documents/Rogers.pdf

Royal College of Psychiatrists. (n.d.) 5 Areas Assessment.
Retrieved from: https://www.rcpsych.ac.uk/healthadvice/treatmentswellbeing/cbt/5areas.aspx

The Counselling Directory. (2013). Integrative Psychotherapy as an Effective Form of Counselling.
Retrieved from: http://www.counselling-directory.org.uk/counsellor-articles/integrative-psychotherapy-is-the-best-approach

UKCP. (2015). Memorandum of Understanding (MoU) on Conversion Therapy in the UK.
Available at: https://www.psychotherapy.org.uk/wp-content/uploads/2016/09/Memorandum-of-understanding-on-conversion-therapy.pdf

Wells A (2019) Breaking the Cybernetic Code: Understanding and Treating the Human Metacognitive Control System to Enhance Mental Health. Frontiers in Psychology, 10(2621). https://doi.org/10.3389/fpsyg.2019.02621


Is there a less colloquial term for the phenomenon known as "brain zaps"? There is an unpleasant phenomenon, colloquially known as "brain zaps".  It is generally associated with withdrawal from antidepressants, but this isn't always the trigger - I sometimes have it even though I've taken my mess that day.

I don't like referring to something so unpleasant and uncomfortable by such a silly name.  Is there a proper medical term for this phenomenon?

Short answer
Brain zaps are a colloquial term for certain symptoms of antidepressant discontinuation syndrome.

Background
'Brain zaps' are associated with sudden shakes, or vibrations, tremors, jolts, electric shocks, or 'zaps' of the head and/or brain. As SydneyMaples rightfully commented, these are scientifically recognized as symptoms of

  Antidepressant discontinuation syndrome, or Antidepressant withdrawal syndrome

Withdrawal from a wide range of antidepressants, including the tricyclic antidepressants (TCAs), monoamine oxidase inhibitors (MAOIs) and selective serotonin reuptake inhibitors (SSRIs) can produce somatic and psychological distress, influenza-like syndromes, gastrointestinal adverse effects, arrhythmias, anxiety, sleep disturbances, movement disorders, mania or hypomania, panic attacks and delirium (Lejoyeux et al., 1996).

Reference
- Lejoyeux et al. CNS Drugs (1996); 5(4): 278–92


How do you predict a cognitive bias theoretically using dual process theory? Disclaimer: I am a complete layman in psychology, with no education in the field whatsoever. This question was prompted by my reading Kahneman's "Thinking Fast and Slow", in which he discusses the model of System 1 and System 2 extensively.

I thought many of the cognitive biases and other psychological effects were fascinating to read about, and I really enjoyed it. But every time he brought the "two systems" into the discussion of a particular cognitive bias (such as the affect heuristic or hindsight bias), it felt like he was using it as a post hoc explanation of how the effect could be described by certain characteristics of the two systems. It was never clear to me how you can show that the dual process implies the existence of the discussed effect.

I think he did a far better job showing how certain psychological effects result from prospect theory. It's easy to show, for example, how prospect theory implies the endowment effect, as shown in the given link. Even though knowledge of the endowment effect existed before prospect theory, it's easy to see how the endowment effect could have been predicted by prospect theory. You can even prove that it would exist, given the utility function of prospect theory and the right axioms.

But I'm confused about how you can do the same with dual process theory, and the cognitive biases that it supposedly explains. How can you use dual process theory to predict the existence of a cognitive bias? Are there examples of cognitive biases that were, or can be explicitly predicted using DPT?

If this is just a poorly framed question--if predicting cognitive biases is not one of the purposes of the theory--then what is the purpose of dual process theory?

EDIT: I want to make a few clarifications here.
My concern is neither with the predictive success of DPT - or other theories to which I compare it - nor is it with whether the things that DPT can predict have already been discovered before DPT. The example I used - prospect theory, and its "prediction" of the endowment effect - is both retroactive (the effect was known before the theory), and according to the answer by Fizz, has questionable predictive verification. However, the manner by which you can use the theory to make the prediction is quite clear. If we assume the value curve given by prospect theory, and the claim of prospect theory that a person's perceived value of a gain or loss is relative to their current position rather than absolutely dependent on the final state, then it follows logically that an individual's perceived gain in value for acquiring something is lower than their perceived loss in value for losing the same thing. This can be answered in theory, on pen and paper, given the framing of the scenario and the axioms of prospect theory.

With dual process theory I want to understand:

what kind of predictions it can make about human behavior
how to make those predictions using the theory

Since this is seemingly a very celebrated modern theory of human behavior, I just want to know how it's used. I don't mind if every known consequence of dual process theory was discovered before the theory, nor do I mind if the method is not as rigorous as that of a physics theory.

Well, whether something is truly predicted or a post-hoc explanation can be difficult to disentangle in this area. What you're asking for is that dual-process theory predicts the existence of a new type of bias previously unobserved. And that's a tall order because observational psychology has been around for a log time.

Probably the area in which I buy the dual-process explanations the most is belief bias; dual-process theory predicts that our intuitions (T-1 processes) bias us for plausible conclusions (and against implausible ones), even if the reasoning (T-2 process) is faulty (and respectively correct).

Predicting an entirely new type of bias is not the only way to test dual-process theory. One can test it quantitatively by looking at known biases and verifying experimentally if the timing affects the level of bias. And in the case of belief bias, that seems to be the case.

The purpose of any scientific theory is to explain some aspect of the real world. Just because we don't continuously discover (qualitatively) new facts based on that theory doesn't invalidate it as scientific theory.

In psychology in general, experimental data is fairly easy to come by, so evidence often leads theory. It's not like in modern physics where you predict the Higgs boson and it takes decades to discover it in actual experiment. Or you predict the string structure of the universe, but it's unlikely we'll ever be able to test that.

By request, here's the introductory / "theoretical" part of the paper:

  [Dual-process] theories posit two distinct
  processes of reasoning that compete for control of the response that
  participants make in reasoning tasks. Heuristic or System1 processes are
  characterised as rapid, implicit, associative, and heavily contextualised,
  whereas analytic or System2 processes are described as slow and sequential
  but capable of abstraction and generalisation. Note that a key difference is
  the speed of processing. The reason for this is that analytic processing is a
  sequential process requiring use of central working memory and is
  constrained by its limited capacity. By contrast, heuristic processes operate
  through massively parallel implicit systems that exert an unconscious
  influence on responding. In support of this distinction is evidence of
  substantial correlations between general intelligence and working memory
  capacity with abstract deductive reasoning but not pragmatic, belief-based
  reasoning (Stanovich, 2004).

  While a mass of evidence has been recorded supporting the idea that there
  are two different processes of reasoning, more research is needed to confirm
  the characteristics that theorists have attributed to the cognitive systems that
  may underlie these observations. A relevant methodological innovation
  reported by Roberts and Newton (2002) is the rapid-response reasoning
  task. The idea is that by constraining participants to respond within a short
  period of time, the slower analytic process of reasoning will be differentially
  inhibited. For example, on the Wason selection task, there is a well established
  non-logical tendency, known as ‘‘matching bias’’ (Evans, 1998),
  to select cards that match the explicit content of conditional statements,
  regardless of the presence of negations. Roberts and Newton (2002) showed
  that measures of matching bias were significantly increased when a rapid response
  version of the selection task was compared with a free-time version.
  This is as dual-process theory would predict, since any influence of analytic
  reasoning to inhibit the bias would be suppressed by the requirement to
  respond quickly.

  A central phenomenon in dual-process accounts of reasoning is that of
  ‘‘belief bias’’—the tendency to evaluate the validity of an argument on
  the basis of whether or not one agrees with the conclusion, rather than
  on whether or not it follows logically from the premises. The
  phenomenon is one of the earliest reported in the psychology of
  reasoning (Wilkins, 1928) but the modern study of the effect dates from
  the paper of Evans, Barston, and Pollard (1983), which established the
  phenomenon with all relevant experimental controls. Evans et al. showed
  that participants’ evaluations of conclusions were substantially affected
  both by the logical validity of the arguments and by the believability of
  the conclusions. With the help of protocol analyses Evans et al.
  characterised the effect as involving a within-participant conflict between
  logic-based (analytic) processes and belief-based (heuristic) processes.
  Such a conflict is to be expected in view of contemporary dual-process
  theories. In support of this, it has been shown that participants high in
  general intelligence are more able to resist belief biases (Stanovich &
  West, 1997) and that logical and belief-based responding are neurologically
  differentiated (Goel & Dolan, 2003).

  In this study, we extend the rapid-response methodology of Roberts and
  Newton (2002) to the study of belief bias in syllogistic reasoning. Using a
  conclusion-evaluation paradigm with problems similar to those of Evans
  et al. (1983), we compare performance under rapid-response and free-time
  tasks. We predict that the participants required to respond rapidly will show
  (a) an increased level of belief bias and (b) a reduced level of logical
  responding.

And regarding prospect theory; quoting from Wikipedia page on it:

  Critics from the field of psychology argued that even if Prospect Theory arose as a descriptive model, it offers no psychological explanations for the processes stated in it.

So I don't see how it is any less of a reverse-fitting of (arguably more math-oriented) description to prior data.

Furthermore, the endowment effect is not even certain to exist, if wikipedia is correct (There are some failed replications, no meta-analysis that I can find.) There are a lot of other (possible) theoretical explanations given for it there as well. In fact there is more theory than there are experiments. Also, being much closer to economics, it's generally more likely to have mathematical models for it.


Can we identify specific emotions on the basis of fMRI scans? I am looking for fMRI studies in which the emotional response of a person listening to music is visible in the fMRI scans, paralleled by a retrospective think aloud report of the person describing his/her emotions while listening. Are there such studies? And did they reveal something comprehensible, i.e. can one see in the fMRI scans how emotions did manifest themselves?

The idea is, that one might be able to distinguish between emotional responses due to characteristic activity patterns or modes, perhaps including the amygdala.

I know of this video with Oliver Sacks being the person, but it disappointed me: we only see that he is emotionally touched stronger by Bach than by Beethoven. But - as I have the impression - we cannot distinguish between positive and negative emotions by just looking at the fMRI scans, can we?

From meta-analyses that include musical emotion inductions, there is not much evidence that we can reliably distinguish between emotions in the brain, independent of the emotion induction procedure or meta-analytical method (1 2 3 4 5).

We might be able to distinguish emotions with specificity and reliability within an individual, but this kind of work is just starting to happen.


Does language learning improve or worsen the ability to remember and process information? In an interview with a Czech neurologist Syka, I've heard that much of the mental health (such as the ability to reason, communicate and process information) in older age mainly depends on the amount of informational ballast we create. The argument states that with this additional information, we unnecessarily wear some of the basic mental mechanisms out (Even though there's no the effect of "too much memories"). Does knowledge of more languages tend to improve or worsen these mental skills?

What I do not quite understand is: What is (according to Syka) "useless information" and how should we "avoid" this kind of information?

Let me try and answer this as follows: During our lifetime, our brain undergoes "synaptic pruning", which lasts from childhood into puberty. Basically, the brain gets rid of "unused" synapses to make space for more complex structures according to the principle of "use it or lose it". It has been hypothesised that sleep has a similar function in that it helps decrease the strength of synapses in order to save energy and not store what you may have referred to as "information ballast" (Synaptic Homoestasis Hypothesis). The creation of new synapses continues throughout our life, which is why there is (some) neural plasticity even in old adulthood. Thus, the brain itself knows how to get rid of irrelevant information (i.e. whatever it does not use) and is receptive to learning even in old age.

What is more, the brain grows with its tasks. So if you avoid learning new tasks, your brain will effectively decline and so will most cognitive skills (working memory, executive functions, processing speed, reasoning etc.). Likewise, our brain does not easily transfer skills from one task to general cognition. If you start doing Sudokus 5h a day, you will improve your Sudoku skills, but not your general ability to reason, for instance. Thus, to the contrary, it seems that what best maintains cognitive functioning in old age is continued engagement in cognitively challenging activities (see Park 2014) rather than the avoidance of new information.

With multilingualism, there is currently a hot debate about its benefits for cognition. For one, it has been shown that bilinguals have a smaller lexicon (per language) than monolinguals - but generally, vocabulary keeps increasing over the lifespan, so I would not worry about that. Ellen Bialystok is a strong defender of the "bilingual advantage", arguing that cognitive skills are even better preserved in bilinguals than in monolinguals, and she provided cross-sectional data showing that symptoms of dementia are delayed by 4 years in bilinguals as compared to monolinguals. The group of Kenneth Paap challenges these findings, arguing that there is no bilingual advantage see Vaughn 2015 for a discussion, but there is little to no evidence suggesting a disadvantage for cognitive ability in bilinguals. Starting to learn a new language in adulthood is even more promising, as it has been shown to promote grey matter increase in areas also responsible for cognitive functions that are known to decline in old age (see Antoniou et al., 2013).

In summary, I do not know of "information ballast" impairing basic mental mechanisms, but knowing more than one language has certainly not been shown to decrease your mental health.


Can a sequence of "automatic" tasks be seen in an EEG? Say I train a task that consists of a sequence of smaller events a 1000 times such that it becomes an automatic/subconscious (something like muscle memory) movement. Then when I view the EEG signal during this automatic task (assuming this task consists of 3 small events) will I be able to see/decode instances of the second and third event once the first event is finished by the user?
It is basically sequential decoding of future automatic events.

The basic answer is that it depends on:

training protocol (duration, frequency)
modality (hearing, seeing, memorizing, attention, etc)
individual variance (observable changes varies between individuals - some may not respond to the training)

So it has to be determined individually for each task (not enough information provided in the original question). In other words, it is an empirical question, which means that the answer lies in the results of an experiment - ”we have to check”.


Laughing as a psychological defense when nervous Say a persons experienced a scarring event in their life (ptsd), and so their mind has developed defense in which they laugh uncontrollably whenever their nervous. This is similar to Joker 2019, whenever Arthur was stressed or depressed he would break out in a laughing episode. However, I began to think otherwise, because later in the film Arthur was physically abused as a child (even being tied to a radiator), which may contributed to this being a physical disorder, but I'm looking for a psychological disorder.

What is the name/term for this condition.

I've thought of psuedobulbar affect (PBA), but after doing research, it is a physical disorder, not purely psychological.

I haven’t seen the movie Joker (2019) ... yet ... but I have observed what is often referred to as nervous laughter occurring with many people, including those involved in the controversial Milgram Experiment (Milgram, 1963) as you can see in this YouTube video at 5 mins 40 secs for example.
There isn’t necessarily any psychological disorder which will cause nervous laughter, but it is a physical reaction to stress, tension, confusion, or anxiety.
Neuroscientist Vilayanur S. Ramachandran states (Ramachandran, 2004):

We have nervous laughter because we want to make ourselves think what horrible thing we encountered isn't really as horrible as it appears, something we want to believe.

and also suggests that laughter is used as a defense mechanism used to guard against overwhelming anxiety. Laughter often diminishes the suffering associated with a traumatic event.
Psychologist and neuroscientist Robert Provine, from the University of Maryland, studied over 1,200 "laughter episodes" and determined that more than 80% of laughter isn't a response to anything he described as “resembling a formal effort at humour” (Provine, 1996).
References
Milgram, S. (1963). Behavioral study of obedience. Journal of Abnormal and Social Psychology, 67(4), 371-378. doi: 10.1037/h0040525 Free PDF: https://pdfs.semanticscholar.org/29e4/8c1365346fc67137423a016096622ac6a215.pdf
Provine, R. R. (1996). Laughter. American Scientist, 84(1), 38-47. Retrieved from: https://www.webcitation.org/67VExLQDj
Ramachandran, V. S. (2004). A brief tour of human consciousness: From impostor poodles to purple numbers. New York, NY: Pi Press.


Power issues with mixed models I'm designing a psychology experiment in which we're interested in how working memory load affects performance in a theory-of-mind task. Independent variable is working memory load, dependent variable is theory-of-mind task performance.

In our within-subjects design, we have 2 working memory conditions (high load and low load). We have 2 stimulus sets (one for each working memory condition, counterbalanced across participants) to prevent carry-over effects between working memory conditions.

The problem is that performance in our task is driven not only by working memory condition, but also by stimulus set to a large extent. My colleague believes this can be dealt with using mixed models. However, I have some doubts about taking this approach, and would rather take the time to adjust the stimulus sets so that performance within each subject is as comparable as possible between both stimulus sets (under the same working memory condition).

If I were to take my colleague's advice, would there be any issues for example with power? And are there resources that you could point me to so that I can understand this issue better?

Edit: There were some questions about sample size and analysis setup. I'm aiming for around 40 participants, but have only just started collecting data.

To clarify, I'm not against using mixed models per se, but I'm wondering: 1) whether there might be a loss in power which is proportionate to the imbalance in effects between the two stimulus types, 2) whether I may need to take steps to compensate for this loss in power, and 3) if so, what steps to take (e.g., is there a way to calculate, roughly, how many more participants I would need given a certain effect size for stimulus type? Or is there perhaps a smarter way to set up the analyses?).

The analysis setup is to perform a linear mixed model, with dependent variable as proportion of correct responses, with fixed effects as working memory load (high vs. low), stimulus type (set 1 or 2), and their interaction, and with mixed effects as intercepts for subjects and items. Then we'd compare this fit with fit of a reduced model without these fixed effects.

I hope this clarifies my question, and appreciate help answering the 3 questions stated in my edit.

Could you maybe check in simulation?
I'm a huge fan of the workflow described here:
https://betanalpha.github.io/assets/case_studies/principled_bayesian_workflow.html

You are asking question #3 of 4, the "inferential adequacy" one, right? Can you run some simulations with varying 'true stimulus-set gap' and just see how big a gap you can tolerate with your design?

You don't need to know the true data generating process to do this, generating responses from the model tells you something useful about the model+design setup, in this workflow reality has to wait until question #4. Also an important question, but checking against reality comes after passing the tests you're talking about.

Although you don't need to know how people actually come up with their responses, you do need to be Bayesian enough to be comfortable putting priors on all the parameters. If it's important to convince a colleague with the results, might be worth checking that's not a dealbreaker for them!


Myer Brigg type for Ni > Ti > Fi > Se I'm reading about Myer Briggs personality types and Jung cognitive functions for the first time.   Based on my understanding, it seems like each of the 16 MB personality profiles attempt to map to some combination of the 8 Jung cognitive functions.

But I can't seem to find an MB profile that maps to the following Jung cognitive function combination

Primary function - Introverted Intuition
Auxillary function - Introverted Thinking
Tertiary function - Introverted Feeling
Inferior function - Extroverted Sensing

Is it because the Jung cognitive function combination I stated is a theoretically and/or practically impossible?  If so, why is that the case?

If you look more into the history of the creators of the Myer's Briggs, you will notice that it is loosely based off Jungian archetypes. It was not created with 16 types initially. Actually, the Jungian theory is only in a few scales (I-E, S-N, T-F), and one of the criticisms of this test is that the theoretical basis really was not preserved.

The combinations you have discussed might not be available, because statistically, it would not have a lot of strength. I would worry about intercorrelated scales, because there is some evidence out there that they are currently, and that does not provide a lot of statistical strength for an actual assessment.

You could further investigate the manual and gain more insight through some of these readings:

Myers, I. Briggs. (2003). MBTI manual: a guide to the development and use of    the Myers-Briggs Type Indicator. 3rd ed. Mountain View, Calif.: CPP.

Capraro, R. M, & Capraro, M. M. (2002). Myers-Briggs Type Indicator score   reliability across: Studies a meta-analytic reliability generalization  study. Educational and Psychological Measurement, 62, 590-602. doi:     10.1177/0013164402062004004

Pulver, C. A., & Kelly, K. R. (2008). Incremental validity of the Myers-Briggs type indicator in predicting academic major selection of undecided university students. Journal of Career Assessment, 16(4), 441-455. doi: 10.1177/1069072708318902


How respected is Viktor Frankl's logotherapy among modern psychologists? Is Viktor Frankl's logotherapy still a live option in modern psychology, or is it considered outdated? I've heard it referred to as the "third Viennese school of psychotherapy", but my wife's introductory psychology textbook (Psychology, 10th ed., David Myers) does not mention Frankl at all.

Is this omission "incidental," or does it accurately reflect a mainstream view that Frankl's work is no longer relevant?

I can't say whether Viktor Frankl is respected by modern psychologists on average, or how respected he is. Anecdotally, I have heard of both Frankl and logotherapy, but not enough to know much more than that they exist. The real question, though, is whether there is any empirical support for logotherapy, and overall, the evidence (for or against logotherapy) I could find is very limited.

Empirical support for logotherapy

At the very least, there has been a limited amount of recent research. Psychometrically, a 2004 review of logotherapeutic measures reported that the Purpose-in-Life test (PIL), the Life Purpose Questionnaire (LPQ), the Seeking of Noetic Goals test (SONG), and the Meaning in Suffering Test (MIST) were internally consistent (Schulenberg, 2004).

Logotherapy also appears to have some empirical support as a treatment for a few specific issues, such as reducing self-reported suffering in adolescents with terminal cancer (Kang et al., 2009), reducing self-reported sense of meaninglessness in people with paralysis (Julom and de Guzmán, 2013), and assisting with the treatment of PTSD (Southwick, Gilmartin, Mcdonough and Morrissey, 2006).

References

Julom, A. M., & de Guzmán, R. (2013). The effectiveness of logotherapy program in alleviating the sense of meaninglessness of paralyzed in-patients. International Journal of Psychology and Psychological Therapy, 13(3), 357-371.
Kang, K. A., Im, J. I., Kim, H. S., Kim, S. J., Song, M. K., & Sim, S. (2009). The effect of logotherapy on the suffering, finding meaning, and spiritual well-being of adolescents with terminal cancer. Journal of Korean Academy of Child Health Nursing, 15(2), 136-144.
Schulenberg, S. E. (2004). A Psychometric Investigation of Logotherapy Measures and the Outcome Questionnaire (OQ-45.2). North American Journal of Psychology.
Southwick, S. M., Gilmartin, R., Mcdonough, P., & Morrissey, P. (2006). Logotherapy as an adjunctive treatment for chronic combat-related PTSD: A meaning-based intervention. American Journal of Psychotherapy, 60(2), 161.


What are the mechanics behind the mind of a conspiracy theorist? Conspiracy Theorists, in my opinion, are people I don't like except for some exceptions. However, this question will not be answered with my irrelevant opinions on said people..

Now, here is the question:

Why do conspiracy theorists become conspiracy theorists?
Why do they get the ideas that they do?
Are they looking for attention?
What are the mechanics behind their minds/thought process?

Some conspiracies:

"Tupac is still  alive, he will come back in year 20(12,13,14)"
"The New World Order is going to take over the world."

Do these people warp things like the Illuminati into a conspiracy? What is behind the minds of these people? Is there any prevalence of mental (conditions, disease) among them? Is there any different type of parenting or environment they are raised in?

All of these questions don't need to be answered, but those are the questions running through my mind.

Interesting question, I am glad that you stated that it is not going to be opinion-based (grounds for closure), as there is some research being done in this field.

A couple papers and details of their research for you:

"Social Psychological Origins of Conspiracy Theories: The Case of the Jewish Conspiracy Theory in Malaysia" (Swami, 2012) states that in some cases, such as the case study presented in the title of this article, it is a 'state-based' conspiracy theory, where:

  in which state-directed conspiracism as a means of dealing with perceived external and internal threats

(emphasis mine).

This could also be extended to why individuals take on the conspiracy theories themselves.

This, in a way relates to the next article:

"The Sarrazin effect: the presence of absurd statements in conspiracy theories makes
canonical information less plausible" (Raab et al. 2013), which is best summed up in one of their concluding paragraphs:

  It is these dynamics of reception, alteration and propagation that account for the many-faceted
  phenomenon we call conspiracy theory. The cognitive effort, i.e., considering information in
  the eventuality space, might be rewarding and satisfying in itself; just like an aesthetic
  experience or a mental exercise (cf. Muth & Carbon, 2013). Unlike a crossword puzzle,
  however, reception and propagation of a conspiracy theory allow for intercommunion. Yet, as
  many participants reported afterwards, constructing a story can ultimately be fun.

Essentially, it is almost like the first example, where the state propagates a conspiracy theory to try to comprehend and cope with perceived threats, the same can apply to the individual.

I hope this helps.


Can an external stimulus change the way your dream ends? I sometimes have the experience that because of a thunder or some other kind of loud sound my dream ends in a way that seems to match with the loud sound. For example, the loud sound of a nearby thunder translates to something making a loud noise in your dream, after which you wake up.

I don't know any scientific evidence of it, but I personally have experienced it many times. I have come to think that it is due to the decreasing depth of sleep. You may know that sleep progresses through different phases. I've read that you only dream during the light sleep phases , or at least you remember to be dreaming during theese phases.
Hearing sound doesn't affect the end of your dream , your brain reacts to the sound with including it in it's own way to your dream at anytime , you just think it's the end of the dream because in that case it wakes you up but your brain does this all night long !

I've already head my alarm ringing in my dreams and it took me several minutes to find out it was realy time to awke up , and not just a background music !

Sorry if it's not scientific enough for you but it seems pretty "normal" to me ^^

EDIT : It seems like people are still trying to prove it but they're convinced it's true : Check this studies results

During the study they observed an impact but due to their lack of technical language the subjects couldn't describe with enough details the impact of internal stimuli on their dream , but new tests will be done with subjects trained with technical language.