Why was MPD changed to DID? Why was Multiple Personality Disorder (MPD) changed to Dissociative Identity Disorder (DID)?

I am currently researching DID and working on an essay relating to its treatment. This change was made from DSM III to DSM IV. I am referencing those two manuals for the treatments and so I was required to explain the terminology change.

DID is one of the most controversial psychiatric disorders, with no clear consensus on diagnostic criteria or treatment.  To answer your question on why MPD was renamed DID, for completeness, there is a bit of history to bear in mind and we will look at the versions of the DSM over the years and how things changed.

The DSM-II used the term Hysterical Neurosis, Dissociative Type. It described the possible occurrence of alterations in the patient's state of consciousness or identity, and included the symptoms of "amnesia, somnambulism, fugue, and multiple personality."

The DSM-III grouped the diagnosis with the other four major dissociative disorders using the term "multiple personality disorder".

The DSM-IV made more changes to DID than any other dissociative disorder, and renamed it DID.

The name was changed for two reasons.

The change emphasises the main problem is not a multitude of personalities, but rather a lack of a single, unified identity and an emphasis on "the identities as centers of information processing".
The term "personality" is used to refer to "characteristic patterns of thoughts, feelings, moods and behaviors of the whole individual", while for a patient with DID, the switches between identities and behavior patterns is the personality.

It is for this reason the DSM-IV-TR referred to "distinct identities or personality states" instead of personalities. The diagnostic criteria also changed to indicate that while the patient may name and personalise alters, they lack an independent, objective existence.

The DSM-IV-TR criteria for DID have been criticised for failing to capture the clinical complexity of DID, lacking usefulness in diagnosing individuals with DID (for instance, by focusing on the two least frequent and most subtle symptoms of DID) producing a high rate of false negatives and an excessive number of Dissociative disorder not otherwise specified (DDNOS) diagnoses, for excluding possession (seen as a cross-cultural form of DID), and for including only two "core" symptoms of DID (amnesia and self-alteration) while failing to discuss hallucinations, trance-like states, somatoform, depersonalisation, and derealisation symptoms. Arguments have been made for allowing diagnosis through the presence of some, but not all of the characteristics of DID rather than the current exclusive focus on the two least common and noticeable features.

The DSM-5 updated the definition of DID in 2013, and the summary of changes listed the changes as:

  Several changes to the criteria for dissociative identity disorder
  have been made in DSM-5. First, Criterion A has been expanded to
  include certain possession-form phenomena and functional neurological
  symptoms to account for more diverse presentations of the disorder.
  Second, Criterion A now specifically states that transitions in
  identity may be observable by others or self-reported. Third,
  according to Criterion B, individuals with dissociative identity
  disorder may have recurrent gaps in recall for everyday events, not
  just for traumatic experiences. Other text modifications clarify the
  nature and course of identity disruptions.


Any ideas about the neural mechanism underlying the ASMR sensation? Autonomous Sensory Meridian Response (ASMR) is described as a pleasurable, tingly sensation in the (back of the) head.
The sensation can be triggered by a vast variety of stimuli (auditory, visual, olfactory etc) but seems dependent on attention. It seems not everyone can get this sensation and among those people that do, stimuli that trigger the sensation vary considerably. See also:
https://en.wikipedia.org/wiki/Autonomous_sensory_meridian_response

But what could be the physical origin of this sensation? And how come only a select group of people seem able to experience it? In http://theness.com/neurologicablog/index.php/asmr/ the ASMR sensation is proposed to be caused by either [1] small seizures or [2] extra sensitivity or extra 'pleasure-shots' to stimuli that for other people are just moderately satisfying. Other sources compare ASMR to meditation.

Does anyone know more about this phenomenon, or have another theory about the mechanism behind it?

I found one study that looked at ASMR and the Default Mode Network (DNM). The DMN consists of the medial prefrontal cortex, medial temporal gyri, bilateral inferior parietal cortices, precuneus and posterior cingulate gyrus. In the study, the DMN of 11 individuals with ASMR was compared with 11 controls.

The DMN of individuals with ASMR showed significantly less functional connectivity than that of controls. The DMN of individuals with ASMR also demonstrated increased connectivity between regions in the occipital, frontal, and temporal cortices, suggesting that ASMR was associated with a blending of multiple resting-state networks. This atypical functional connectivity likely influences the unique sensory-emotional experiences associated with ASMR.

Reference:

D. L. (2008). The brain’s default network: Anatomy, function, and relevance to disease. Annals of the New York Academy of Sciences, 1124, 1–38. doi:10.1196/annals.1440.011


What is the longer term prognosis for women in their early 20's with Schizoaffective disorder? I am asking as I have this condition and I am hoping to gather more data about my particular demographic, in order to give me a better idea as to what they are doing, as well to lead me to how those of us with this condition fare later in life.

What is the long-term prognosis for schizoaffective disorder?

Note, this is not my area, and not medical advice. If you need help with this you should consult an appropriately trained health practitioner.

To consult the scientific literature, do a search like "schizoaffective disorder prognosis" on Google Scholar.

For example, Robinson et al (1999) provide some relevant empirical data. The sample was 50% female and had a mean age of 25.6 (SD=6.3) years. To quote their abstract:

  Background  We examined relapse after response to a first episode of
  schizophrenia or schizoaffective disorder.

  Methods  Patients with first-episode schizophrenia were assessed on
  measures of psychopathologic variables, cognition, social functioning,
  and biological variables and treated according to a standardized
  algorithm. The sample for the relapse analyses consisted of 104
  patients who responded to treatment of their index episode and were at
  risk for relapse.

  Results  Five years after initial recovery, the cumulative first
  relapse rate was 81.9% (95% confidence interval [CI], 70.6%-93.2%);
  the second relapse rate was 78.0% (95% CI, 46.5%-100.0%). By 4 years
  after recovery from a second relapse, the cumulative third relapse
  rate was 86.2% (95% CI, 61.5%-100.0%). Discontinuing antipsychotic
  drug therapy increased the risk of relapse by almost 5 times (hazard
  ratio for an initial relapse, 4.89 [99% CI, 2.49-9.60]; hazard ratio
  for a second relapse, 4.57 [99% CI, 1.49-14.02]). Subsequent analyses
  controlling for antipsychotic drug use showed that patients with poor
  premorbid adaptation to school and premorbid social withdrawal
  relapsed earlier. Sex, diagnosis, obstetric complications, duration of
  psychotic illness before treatment, baseline symptoms, neuroendocrine
  measures, methylphenidate hydrochloride challenge response,
  neuropsychologic and magnetic resonance imaging measures, time to
  response of the initial episode, adverse effects during treatment, and
  presence of residual symptoms after the initial episode were not
  significantly related to time to relapse.

  Conclusions  There is a high rate of relapse within 5 years of
  recovery from a first episode of schizophrenia and schizoaffective
  disorder. This risk is diminished by maintenance antipsychotic drug
  treatment.

References

Robinson, D., Woerner, M. G., Alvir, J. M. J., Bilder, R., Goldman, R., Geisler, S., ... & Lieberman, J. A. (1999). Predictors of relapse following response from a first episode of schizophrenia or schizoaffective disorder. Archives of General Psychiatry, 56(3), 241. FULL TEXT


Is Melatonin necessary to sleep? Consider a scenario  where a person's melatonin secretion gets inhibited (and that person also don't get external melatonin);

Will this person feel sleepiness and a desire to sleep? Or, since that person is not having melatonin being secreted, there will not be any sleepiness?

Searching for this, I found that "melatonin levels in the blood rise sharply and you begin to feel less alert". However, I would like to know if a person which is not have melatonin being secreted will not feel sleepiness.

Is Melatonin necessary to sleep or even to have desire for sleep?

I don’t have a direct or a very reputable reference to answer this question, but I work in the clinical field and have seen many insomniacs, so I’ll offer you the answers based on the references and the experiences I have for you to consider in the meantime.

Melatonin’s principal function is to convey the message of darkness or information about timing of the day and night to the central circadian clock. [1-3]

  In mammals, a central circadian clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, tunes the innate circadian physiological rhythms to the ambient 24 h light–dark cycle to invigorate and optimize the internal temporal order. … Melatonin conveys the message of darkness to the clock and induces night‐state physiological functions, for example, sleep/wake blood pressure and metabolism. [1]

and

  The primary physiological function of melatonin, whose secretion adjusts to night length, is to convey information concerning the daily cycle of light and darkness to body structures. [2]

Melatonin does not have direct effects on sleep-wake cycles, which are governed by other complex neural circuits in the brainstem. It is not one of the neurotransmitters in the complex sleep-wake neural circuits, which utilize cholinergic, noradrenergic, and serotonergic neurotransmitters. Melatonin just influences the circuits by conveying the message of darkness or timing of the day and night to the SCN, the central circadian clock, which in turn, affects the sleep-wake neural circuits.

  The highly organized sequence of human sleep states is actively generated by nuclei in the brainstem, most importantly the cholinergic nuclei of the pons–midbrain junction, the noradrenergic cells of the locus coeruleus, and the serotonergic neurons of the raphe nuclei. The activity of the relevant cell groups controls the degree of mental alertness on a continuum from deep sleep to waking attentiveness. These brainstem systems are in turn influenced by a circadian clocks located in the suprachiasmatic nucleus and VLPO of the hypothalamus. The clock adjusts periods of sleep and wakefulness to appropriate durations during the 24-hour cycle of light and darkness that is fundamental to life on Earth. [4]

Clinically, melatonin seems to be neither necessary nor sufficient for sleep to occur. This is evident by the fact that when melatonin is high in the night and a person is about to fall asleep or even asleep, he /she can be awakened and remain awake by some strong stimulus despite the high level of melatonin at that time. Also, if melatonin is given to awake people, they may feel like sleeping, but, unlike strong sleeping pills (which mostly affect cholinergic, noradrenergic, and/or serotonergic neurotransmissions), they may not fall asleep if other things such as surrounding circumstances do not allow them to sleep. So, melatonin alone is not sufficient for sleep to occur or be maintained.

On the other hand, when a person is deprived of sleep for one or more nights, he/she can fall asleep during daytime even if the level of melatonin is low at that time. Or, if strong sleeping pills (which mostly affect those mentioned neurotransmissions) are given to awake people during daytime, when melatonin level is low, they will fall asleep despite the low level of melatonin. So, melatonin alone is not necessary for sleep to occur or be maintained.

In summary, the principal role of melatonin regarding sleep is to convey the message of darkness or information about timing of the day and night to the central circadian clock to influence the sleep-wake neural circuits so that the animal, including human, can sleep at appropriate time; but it is not necessary or sufficient for sleep to occur or be maintained.

References.

Nava Zisapel. New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation. Br J Pharmacol. 2018 Aug; 175(16): 3190–3199.
Claustrat B, Leston J. Melatonin: Physiological effects in humans.. Neurochirurgie. 2015 Apr-Jun;61(2-3):77-84. doi: 10.1016/j.neuchi.2015.03.002.
Pandi-Perumal SR1, Srinivasan V, Spence DW, Cardinali DP. Role of the melatonin system in the control of sleep: therapeutic implications. CNS Drugs. 2007;21(12):995-1018.
Purves D. Chapter 27.  Sleep and wakefulness. Neural circuits governing sleep. In Neuroscience. 3rd ed. Sunderland, Massachusetts: Sinauer Associates Inc; 2004. p 674-684.


How important is eye contact for attraction between a man and woman? How important is eye contact for creating/inducing attraction & showing showing "confidence" towards them?

What is the optimal eye locking duration between 2 persons for inducing this attraction?

While eye contact is certainly important in social interaction I think you should beware pseudoscientific dating advice based on manufacturing "attraction" between men and women. Since this site is about science, let me point to a couple of areas of empirical research looking at eye contact.

First, there are quite a few experimental papers showing that (pictures of) faces with direct gaze (looking towards you) capture and hold attention, are remembered better, and that they are rated as more attractive. For details see this pdf. There are other similar papers.

Second, there is a long tradition of looking at gaze in non-verbal behaviour. Basically, although this shows that people are sensitive to direct gaze it is only one of many cues related to conversation etc. A classic review is here. Interestingly, the timing of direct gaze (when you look and when you look away) is very important in conversation.

This suggests to me that both looking at someone too long, and not looking at them enough or at awkward times, can cause interactions to suffer. Atypical eye contact is a diagnostic criterion for autism, which is normally associated with difficulties in socialising.


Analyze subconscious/unconscious scientifically Is there a way to analyze human subconscious/unconscious scientifically in some way? I mean for example to help me better understand my fears, insomnia etc.

There are many people out there who offer courses for $$$ that claim things to "reprogram your unconscious" to help achieve (personal) goals etc. Usually these courses only involve talking to a coach and let him guide you/let you realize what is right/wrong for you. I am suspicious that if clients of those courses claim the got some benefit it may have only been that they shelled out big $s which helped them to realize they actually do not need to spend $s and only maybe talk to a friend to achieve easy things like eating too much etc.

I wonder if there may be a real scientific theory or procedure that would say - hey, there is this or that activity on your EEG (or "you say you had/are having these/those dreams"), you seem to have suffered by -whatever- in your childhood and you should/should not do this and that to straight it out (or minimize) in your adolescence.

Those courses you mention are a part of a much larger "personal development" market that really boomed in the 90s, and keeps going on ever since.
There's a book called "Letting go: a pathway of surrender" and the part that really jumped at me is that the author lists dozens of different flavors of that "personal development" offerings:

“Well,” you say, “there have to be some experts who have the answers.” When upset, you go to a doctor or psychiatrist, an analyst, a social worker, or an astrologer. You take up religion, get philosophy, take the Erhard Seminars Training (est), tap yourself with EFT. You get your chakras balanced, try some reflexology, go for ear acupuncture, do iridology, get healed with lights and crystals.
You meditate, chant a mantra, drink green tea, try the Pentecostals, breathe in fire, andspeak in tongues. You get centered, learn NLP, try actualizations, work on visualizations,study psychology, join a Jungian group. You get Rolfed, try psychedelics, get a psychicreading, jog, jazzercise, have colonics, get into nutrition and aerobics, hang upside down, wearpsychic jewelry. Get more insight, bio-feedback, Gestalt therapy.
You see your homeopath, chiropractor, naturopath. You try kinesiology, discover yourEnneagram type, get your meridians balanced, join a consciousness-raising group, take tranquilizers. You get some hormone shots, try cell salts, have yourminerals balanced, pray, implore, and beseech. You learn astral projection. Become a vegetarian. Eat only cabbage. Try macrobiotics, go organic, eat no GMO. Meet up withNative American medicine men, do a sweat lodge. Try Chinese herbs, moxicombustion,shiatsu, acupressure, feng shui. You go to India. Find a new guru. Take off your clothes. Swiin the Ganges. Stare at the sun. Shave your head. Eat with your fingers, get really messy,shower in cold water ........

The point is that there are thousands of people out there who would be happy to take your money to tell you about your problems and subconscious. :)
From what I understand, EEG is very difficult to analyze, and does not have the accuracy that you are seeking.
From my personal experiments, observing the intensity and content of dreams may offer some insight into one's subconscious, however it is extremely subjective.


How much information is lost when conveying an experience or emotion to another person? Certain languages have words that do not literally translate into any another language.  There is already a small loss of information in this sense.

Emotions are a personal experience and the gravity and meaning of them are dependent on the person who experiences them.  The same goes for all conscious experiences.

So how much information is lost when one person is trying to convey these personal experiences with another person?  Will actions carry more relevant data than words when explaining a personal experience?

Is there any way to quantify the loss in translation of experiences?

Communication is always a lossy and inexact process. If I am trying to convey information to you - the times of trains, for example - I can use dates and times that I can be confident that you will interpret the same way I do. But you may not - I may say the train leaves at 8:40, and you assume I mean the morning, whereas I actually mean the evening. So while there is a consistent and standardised worldview that I share, I can have reasonably high confidence in this.

When it comes to emotions, these are, by definition, more subjective. The shared worldview is much smaller, and the chances of the words having the same meaning between us is significantly less. Because most words actually have emotional resonances, there is always this danger, but when the emotional resonance is the intention, this is an issue. I can only be sure of communicating the emotions to you if we share the same emotional language.

This language is build though our experiences, memories, make-up etc, so to share a language, we need to share all of this - effectively impossible. To measure the difference, we would need to do a substantial comparison of the relevant worldviews of the two communicants. Given that most people cannot even start to quantify their own dominant worldview, this does not seem likely.

Just noted - you referred to experiences not emotions. However the same applies, because our experiences are communicated emotionally.


Is there a standard list of Default Answers which are used in Likert 'type' Scales I have always had some trouble deciding what to use as the default answers when using Likert 'type' scales.

Is there a default list of accepted answers to particular types of questions which are used by survey designers? e.g. "Level of effect", "Amount you agree with",  "Make you act" "Level of Awareness" type questions.

I accept that there is a huge range of types of questions but if there was some sort of semi standardised list of 5, 6 and 7 point answers it would be very handy. In many cases I have difficulty thinking of just one of the answers or the correct terminology or syntax which should be used to ensure that each of the answers are 'appropriately distributed'... if that makes sense

For many types of questions there are existing examples online e.g.

  What most clearly reflects your political leaning?

  Strong Democrat
  Not so strong Democrat
  Independent leaning Democrat
  Independent
  Independent leaning Republican
  Not so strong Republican
  Strong Republican
  Other
  Don't know

Or

  The county is on the right economic path

  Strongly agree
  Agree
  Neither or N/A
  Disagree
  Strongly Disagree

However in other instances it is more difficult to figure out what answers should be used

  In your opinion, does a perceptible level of bias in a particular news
  story affect the overall level of credibility the story has?

  Yes, most definitely
  Yes, to some degree
  Yes, a slight effect
  No, ????
  No,not really
  No, not at all

Any help or links to resources would be seriously appreciated. Thanks

Here are links to several lists of common Likert-type response anchors (the first link provides a nice variety):

http://www.clemson.edu/centers-institutes/tourism/documents/sample-scales.pdf

http://www.rpgroup.org/sites/default/files/Surveys%20Interactive%20Activity%20-%20Examples%20of%20Likert%20scales.pdf

And these links provide suggestions regarding designing these scales and may help you determine how to adapt the anchor options from the first set of links:
http://www.uwex.edu/ces/4h/evaluation/documents/wordingforratingscales.pdf

http://surveynet.ac.uk/sqb/datacollection/likertfactsheet.pdf

http://academics.lmu.edu/spee/officeofassessment/surveysevaluation/surveydesign/step3determinetheformatoftheresponseoptions/

http://www.dism.ssri.duke.edu/pdfs/Tipsheet%20-%20Response%20Scales.pdf


Psychological theories about the end of a romantic relationship There's no doubt: many couples break and many marriages break, what happens in these cases?

In the loving encounter brain areas aimed at judgment and critical analysis, are clouded by an increase of dopamine: the neurotransmitter that activates our most irrational and euphoric drives.
The biology tells us that this pleasant situation lasts a few months (activation of oxytocin receptors) because of the decrease of dopamine in the intersynaptic space.

Which other theories could explain the decline in desire/closeness?

Does exist a split between desire and love?

References:

Massimo Recalcati (2014) "Non è più come prima", Milano: Raffaello Cortina Editore
Michael S. Gazzaniga, Richard B. Ivry, George R. Mangun (2015) Neuroscienze cognitive, Zanichelli.

Is there a split between desire and love?

Of course, love and lust/desire are two completely different things.
A simple definition I have of the word love:  An involuntary response to virtue.

This obviously means I can't "love" someone without knowing whether or not they are honest, benevolent, or have integrity.  It also means that I can't love someone if I am morally corrupt, because doing so would expose my corruption.  To protect myself, I would be repulsed from that person.

Lust, of course, is biologically programmed in our brain and nearly impossible not to experience, unlike love.  I can scarcely be attracted to a woman, go on one date with her, and conclude that I love her.

Like you said, dopamine and other chemicals in the brain can cloud our judgement and lead us to believe we love someone and ignore their red flags for negative behaviors like abuse, when we are merely biologically driven to reproduce with them.  I have heard that this euphoria lasts for about six months until desire fizzles and romantic interest is lost by someone and the relationship ends.

Which other theories explain the decline in closeness?

Abuse of all kinds.  Verbal, physical, and sexual abuse cause big problems, particularly if the abuse is at a young age.  Simply spanking children has been conclusively found to reduce empathy and IQ and increase "brain disorders."  With this information available, more than 80% of American parents still spank their children!  From Christian culture, to Tongan culture, to Muslim culture, spanking and abuse is the norm.  How can we be close to someone if we cannot empathize with them?  Empathy is the deepest level of understanding we can have for someone at any point in time.

I would argue that we are increasingly trying to ignore our unconscious responses to trauma and grief, particularly as children, in society.  The problems are ignored by parents with empathy and emotional distance from their kids which allows them to spank their children and let depression and other problems that could be significant, go unnoticed or even criticized. Endless amounts of "culture propaganda" about how parents are inherently good and loving people despite their abuses, and schools that are teaching kids what to think instead of how to think & solve problems only exacerbate the problem.

Depression and substance abuse is a natural and valid response to events that are usually traumatic - childhood sexual abuse is just one example.  These valid responses in our brain are being labeled with "brain disorder" diagnoses and antidepressants when the unconscious brain is doing exactly what it was designed to do - Warn us that something is wrong.  The benefit for this is obvious.  Just look at the millions of dollars worth of advertising spent for antidepressants on American television.  Often victims are told something is wrong with them, when more often than not, someone wronged them.

Instead of finding the problems in our past that have contributed to unhealthy lifestyle patterns through therapy or self-knowledge work, we, with the help of our "what to think" education, run to the nearest "answer" - a mind-altering drug and a label for our problem.

A closer look at how ignoring the truth can affect society as a whole...

Biologically speaking, as children we are genetically designed to understand that our parents are biologically successful.  They reproduced.  We grow up and learn patterns of behavior from parents in order to be biologically successful based on their success.

Generally speaking:

A boy will model general behavior patterns in his father and be attracted to the general behavior patterns found in his mother
A girl will model general behavior patterns in her mother and be attracted to the general behavioral patterns found in her father

Patterns can be categories such as honesty, empathy, integrity, etc.

For example, children that grow up without a father (exception: children of widowed mothers) experience:

Increased promiscuity
Increased likelihood of committing crimes, violence, and abuse
Increased aggression
Increased teen pregnancies
Increased likelihood of being abused
Increased likelihood of divorce

This is an example of two parents that had an apparent lack of empathy for their children.  It is important to remember that empathy is taught behavior and instead of empathy, they were largely traumatized and abandoned.  The boys absence of a father leads them to have less empathy, shown through crimes and violence against other people.  The pattern often repeats through promiscuity and teen pregnancy and can extend to other families through crime.

I think the evidence suggests that poor parenting choices, whether directly or indirectly, is deteriorating our closeness, community, and ability to love and empathize. How long before the unabused outnumber the abused?  That, I believe, is up to us.

Sources (unfortunately can only do 2 links):

Single Mother Childhood (additional sources)

Facts About Spanking (additional sources)

Search "sins of the father" on the same channel for a firsthand abuse story

Search "confessions of a womanizer" on same channel for a firsthand story from a cheater!

Search "an honest conversation with a single mother" on same channel for a firsthand story from a single mother


What is the relationship between dopamine and mathematical ability (if any)? I am curious to know if there is any existing literature that suggests that an increase in dopamine lends itself to an increased interest in solving problems of a mathematical nature.

A study Evidence that methylphenidate enhances the saliency of a mathematical task by increasing dopamine in the human brain suggests that using of Methylphenidate that is prescribed for attention deficit hyperactivity disorder (ADHD) increases the performance in mathematical tasks in healthy subjects. Methylphenidate primarily acts as a dopamine-norepinephrine reuptake inhibitor.

  Methylphenidate, when coupled with the mathematical task,
  significantly increased extracellular dopamine, but this did not occur
  when coupled with the neutral task. The mathematical task did not
  increase dopamine when coupled with placebo. Subjective reports about
  interest and motivation in the mathematical task were greater with
  methylphenidate than with placebo and were associated with dopamine
  increases.


Do the results of psychological studies change our behaviour? This is a question that has been bugging me for a very long time.

Let me illustrate with a silly example. Suppose that a study finds out that the majority of the population associate the number 1 with the colour blue (again, this is is a very silly example). Suppose this study becomes very popular and the result comes to be known to most people. How will this knowledge of the experiment change behaviour?
Will the result still be the same after the study is known to the entire population?

EDIT :
I am not talking about the kind of results where we do not have influence on our behaviours, like our heart rate during a tense situation or how we react when our life is threatened. I am talking about experiments where we can make a conscious choice and is apparently "inconsequential" (so, nothing that poses harm to us).

EDIT 2:
//New Example//
The use of canned laughter in sitcoms -- Many of us by now have realised that laugh tracks are used in sitcoms to direct how the audience should react and make them think that what they are watching is funnier than it actually is (Example of Social Proof, which is nicely explained by Robert Cialdini). After I knew this, I actually found TV shows employing the technique to be less funny and in some cases, even annoying. (I assume that many people reacted the same way after finding out about it).
So the study of this particular behaviour actually made me react in the opposite way that the TV show producers intended and how the study says I should be behaving. Thus, changing the results of the study.

Are there other studies like this? How do we design experiments that are tolerant to this?

I do have to note this question is broad and opinion based, according to the stack conventions. Nonetheless, I think it's an important question, given that scientific publications may alter the behavior of people en mass and even generate entire movements that, e.g., argue and campaign against vital medical interventions.

A notorious example being the retracted Lancet publication of the adverse effects of vaccination causing autism, based on fraudulent data (Rao & Andrade, 2011) by Wakefield (1998). This unfortunate paper has resulted in global anti-vaccine movements based on the fictional assumption that vaccination can cause autism.

References
- Rao & Andrade, Indian J Psychiatry (2011); 53(2): 95–6
- Wakefield et al., The Lancet (Retracted)


How do the correlations between Big 5 personality change in studies examining "faking bad"? I have conducted several studies that get participants to complete the IPIP personality test while role play going for a job. A common finding is that the average correlation (i.e., $\bar{r}$ between big 5 personality scales increases the more you ask people to fake.
For example, the rough pattern in the data is:

Get participants to complete a personality test honesty ($\bar{r} = .25$)
Get participants to complete do a job applicant role-play ($\bar{r} = .40$)
Get participants to complete a job applicant role-play and explicitly tell then to fake it ($\bar{r} = .60$)

Thus, increasing the amount of faking, increases the average intercorrelation.
I'm interested in what happens when participants "fake bad" (e.g., specifically try to present a negative impression such as depressed, disturbed, or socially undesirable).

What have previous studies found to be the effect of "faking bad" on the average scale intercorrelations of Big 5 personality?
Have any researchers offered theoretical explanations for any observed effect of faking bad on such changes average scale intercorrelations?

I don't know any actual "faking bad" studies or theories involving the Big Five, but there are some theories about the Big Five's general factor that can both explain the common finding you mention and inform a hypothesis about potential results from a study that would address your questions. I don't expect this will be a very satisfying answer, because I'm offering it in a bit of a hurry and referencing your own questions (and answer) to provide referential substance, but here it is anyway.

As your question and answer point out, there is a general factor underlying the Big Five, an even bigger "Big One." It partly reflects social desirability, as you know from your other question, and partly reflects people's efforts to align their personalities (or at least their opinions about their own personalities) toward those more desirable poles of the dimensions. It may even reflect some adaptive advantage to being slightly toward the desirable side of average (though probably not all the way to the extreme end of that side). Whether people succeed at being these desirable, maybe better-adjusted versions of themselves in the long term is immaterial. They try in the short term, and tell themselves it's working for various reasons, including self-serving bias and self-perceptive processes in identity (that inform judgments with recent behaviors).

People have some intuitive sense of the desirability of being sociable, stable, friendly, responsible, and curious (not to mention other aspects of each trait). If asked to act like a professionally desirable (i.e., hire-worthy) applicant, they will bias their answers in these socially desirable directions. These biases (whether intentionally deceptive or unconsciously ego-defensive) partly overlay some of the natural, independent variation with an internally consistent personality profile that suits the social consensus of what is desirable. Therefore people seem more uniform and correlations strengthen. Maybe you know other explanations of this finding as well; this may be one explanation, but I doubt it's the only.

I think this explanation could apply equally well if people were asked to "fake bad." Again, a socially undesirable personality profile is socially salient and consensual enough to overlay natural, independent variation with a relatively uniform pattern of bias. Most people know you're probably less likely to get hired if you act shy, edgy, hostile, impulsive, and stubborn (again, among other things that generally point in the same overall directions more often than not). Therefore I'd expect increased correlations in the "faking bad" scenario too.

Not a well-researched theory here I'm afraid; just a hypothesis or half-educated guess. I hope it's helpful nonetheless, and would be happy to look further into it and edit if anyone's interested enough to comment on a pseudo-answer that's nine months late. I can definitely offer some references for at least some of the instrumental points of theory I offer here without explicit support if that's socially desirable enough!


Why does staring at a single point make it easier to balance on one leg? If I'm trying to put a shoe on while standing with one leg, it's easier to maintain balance while staring at a single point (e.g., on the ground).

Why does staring at a single point make it easier to balance on one leg?

Vision and balance are linked
Balance is fluid:
Vision and balance are connected within the brain. Balance is not something that the brain determines, is learned, "this way is up" and never revisited- like this smell = coffee, this sound = a bird; it is a continual process of biofeedback.
Three aspects of balance: vestibular system, vision and proprioception

Balance is the result of several body systems working together: the visual system (eyes), vestibular system (ears) and proprioception (the body's sense of where it is in space). Degeneration or loss of function in any of these systems can lead to balance deficits

We use our surrounds as a frame of reference, for our internal spirit level.  Maintenance of an accurate spirit level  involves continual measurement and feedback between the visual and vestibular systems, they are connected via the vestibulo-ocular reflex. When vision remains fixed upon an object, balance is achieved by the eyes moving to  counteract   the body's movements. These processes are interdependent, happening simultaneously, as the neurons that are stimulated within the visual system causing the neurons within the vestibular system to fire and vice versa.
Or simply put; Movement  is detected by the vestibular system, and the eyes give a plane of reference, offering proprioception.
It could be likened to axes on a graph, and both dimensions (vision and vestibular) are needed to plot the point of proprioception.
Vestibulo-ocular reflex:

The vestibulo-ocular reflex (VOR) is a reflex eye movement that stabilizes images on the retina during head movement by producing an eye movement in the direction opposite to head movement, thus preserving the image on the center of the visual field. For example, when the head moves to the right, the eyes move to the left, and vice versa. Since slight head movement is present all the time, the VOR is very important for stabilizing vision: patients whose VOR is impaired find it difficult to read using print, because they cannot stabilize the eyes during small head tremors. The VOR does not depend on visual input and works even in total darkness or when the eyes are closed.

Image courtesy of http://en.wikipedia.org/wiki/File:Vestibulo-ocular_reflex_EN.svg
An integrated view of balance:

The vestibular system works with other sensorimotor systems in the body, such as the visual system and proprioceptors in muscles and joints to check and maintain the body’s position at rest or in motion. These systems enable individuals to maintain a steady focus on objects even when body position changes and to safely maneuver in the environment.
The visual system specifically interacts with the vestibular system via the vestibular-ocular reflex, which senses head movements and generates equal and opposite eye movements to maintain image stability on the retinal fovea. The visual system is thought to provide continuous feedback about any retinal slip and the need to recalibrate the vestibulo-ocular reflex. (UC Davis Health System)

As we read and move our heads, our gaze is held steadily and we are able to continue reading uninterrupted thanks to the VOR. Given any alteration within the visual system, results in an alteration in our vestibular system and vice versa; when attempting a task that requires difficulty in maintaining balance, if the vision remains steady, as in constant upon an object, the vestibular system is able to measure (or locate)  the body's  proprioception and make adjustments to keep the vestibular system in the required plane (like the spirit level being kept level). So the effect is, we have one constant, vision and two variables; vestibular and spatial awareness.
Given the fluid nature of how the brain achieves balance; if the eyes were flitting and the visual field was varying, we have three variables. Mathematically this becomes a more complex formula for the VOR to determine where the body is spatially.
Interestingly, uncorrected poor vision can also cause poor balance when the eyes are closed.

... visually impaired individuals and those with uncorrected refractive error — those who could benefit from glasses to achieve normal vision but don’t wear glasses — have a significantly greater risk of diminished balance with their eyes closed on a compliant, foam surface than individuals with normal vision. (UC Davis Health System)

The link between balance and vision is an area of ongoing research.

References:

The Human Balance System
GOOD BALANCE IS OFTEN TAKEN FOR GRANTED
Vestibular Disorders Association

Common Conditions/Symptoms Associated with Vision
Brain and Eye Connection
Vision Clinic

Queensland University of Technology
Faculty of Health
Vision, Balance and Falls

How Our Balance System Works
American Speech-Language-Hearing Association


Can "fire together, wire together" be undone? Are new connections continuously forged in the adult human brain, or do we just start all wired together and then prune until we have something we like?

The phrase "fire together, wire together" comes from an explanation of Hebbian Learning and refers to the adaptation of synapses as a response to the firing of already connected neurons. This is one of several Synaptic Plasticity mechanisms. Two others that exist are Long Term Potentiation (strengthening and creation) and Long Term Depression (weakening and destruction).

All of these mechanisms are still being researched heavily to understand their detail better. However, I hope this gives you a good starting point.


Length of neuro-physiological signals of emotion compared to feeling time In "Determinants of Emotion Duration and Underlying Psychological and Neural Mechanisms" by Verduyn et al. discuss how certain physiological signals are outlasted by actual feelings:

  In particular, whereas the duration of expressive
  (e.g., facial expression; [1]), and (neuro)physiological components
  (e.g., cardiovascular recovery; [2]) seems to rarely exceed a few
  minutes, feelings and associated cognitions may persist for hours or
  longer (e.g., [3], [4]).

Is this true for all external physiological signals including Galvanic Skin Response (GSR) and Electromyography (EMG)? I would find this surprising given that there is evidence of the central nervous system being related relating physical to social pain, as shown in "Acetaminophen Reduces Social Pain: Behavioral and Neural Evidence" Dewall et al., so I would expect some external evidence of this physical pain.

[1] Ekman, Paul, and Wallace V. Friesen. "Felt, false, and miserable smiles." Journal of nonverbal behavior 6.4 (1982): 238-252.

[2] L. Fredrickson, Barbara, and Robert W. Levenson. "Positive emotions speed recovery from the cardiovascular sequelae of negative emotions." Cognition & emotion 12.2 (1998): 191-220.

[3] Nolen-Hoeksema, Susan, and Jannay Morrow. "Effects of rumination and distraction on naturally occurring depressed mood." Cognition & Emotion 7.6 (1993): 561-570.

[4] Verduyn, Philippe, Iven Van Mechelen, and Francis Tuerlinckx. "The relation between event processing and the duration of emotional experience." Emotion 11.1 (2011): 20.

In "Simultaneous acquisition of corrugator electromyography and functional magnetic resonance imaging: A new method for objectively measuring affect and neural activity concurrently" Aaron et al. use face EMG to measure emotional reaction to photos. As shown in the figure below, the response only lasts a few seconds:

Getting a GSR response is more complicated due to the noise in the reading. In "Time-series analysis for rapid event-related skin conductance responses" by Bach et al., the authors figure out a mathematical approach for figuring out the event-related response. Both via a smoothed fitted gamma distribution and PCA component analysis are used below:

Both response measures seem to return to reference levels after 30 minutes.


Cognitivism over Behaviorism While reading up on the differences between cognitivism and behaviorism, I came across this:

  Cognitive science, however, overcomes Behaviorism’s main faults,
  particularly that reflexes and reinforcements cannot account for all
  human behavior and that animal behavior is not the best predictor of
  human behavior.

https://woknowing.wordpress.com/2010/10/12/behaviorism-vs-cognitivisim/

Could you give some concrete examples of such behaviors that behaviorism fails to account for and where cognitivism can?

let's have a look at the social cognitive theory by Bandura:
It says, that behavior can be acquired by simply watching other people act on something. Maybe you have already heard of the famous bobo-doll experiment, if not here is a link:
https://www.youtube.com/watch?v=128Ts5r9NRE
Anyway: behaviorism doesn't care about anything going on inside our mind, like reasoning for example. It simply breaks behavior down to stimulus-response-mechanisms or behavior-response-interactions, that is why behaviorists call the mind a "black box". They simply think in a way of Input-Output mechanisms, the thing in between these two gets neglected.
So, going back to the social cognitive theory: Behaviorists can't explain behavior, that was acquired through observing other people. The person, who is the observer, has never experienced something like a stimulus-response trial, or acted on the behavior on his own. However, we know that it is possible and people need something like a memory, perception, reasoning, to learn in such a way. So, we need cognitive abilities to explain this kind of behavior (we have to look inside the black box), which is incompatible with behaviorism.

In other words: every behavior, that needs or was being activated by something, that is a part of our cognitive abilities, is a behavior, that can't be explained by behaviorism.

Another example is problem solving: To solve a problem, we think about the situation, reassemble the elements and then act. Behaviorism can't account for such a behavior.


How do people perceive subjective scales? Let's take a picture of apples:

Are there experiments conducted that study the distribution of the following answers to the question "How many apples are on this picture?":

Very little
Little
Normal
Many
Lots of

Well, of course, this specific picture doesn't matter, but this type of questions is important for many applications, like in surveys, when people rate things on subjective scales, so that in particular situations we can compare neither across questions with the same scale nor across persons answered the same question.

For example, think of 360-degree surveys when a person rates himself and is rated by others, so to compare in the end the two ratings.

If I understand you correctly, you are trying to learn about good practice in designing studies involving subjective scales? Then getting actual answers to such surveys might not be very helpful. You might rather want to know the impact of your survey design and the answering-environment on the answers of the respondent.

These are broad questions. Neither do I have the expertise nor the space to give you comprehensive answers here. Some suggestions though. As far as study design is concerned, you may want to consult Survey Methodology. In particular, section 5.3.5 deals with the implications of the type of scales used as possible answers. In fact, any other Survey Methodology textbook should cover this topic.

A lot of experiments also study the impact of social environment on perceptions and the construction of subjective opinions. Among others, Solomon Asch is a pioneer of experimental investigations of subjective perception. His most famous experiment is related to the conformity effect. He shows that people tend to conform to the perception of the group they are put in, even when this goes against strong visual evidences, see http://www.youtube.com/watch?v=FnT2FcuZaYI.

In another famous experiment, Asch studied the "recency" and the "primacy" effect. The subject of the experiment where enumerated a list of personality traits (generous, peaceful, wise, mean,...) and subsequently asked to described the person. Asch question was whether, in describing the fictitious individual, people would rely more heavily on the first enumerated traits (the "primacy" effect), or would rather focus on the last ones they where presented (the "recency" effect). Asch results tend to show a dominance of the "primacy" effect.

Again, it would be too long to present a list of the numerous experiments and theoretical attempt to grasp perceptions mechanisms here. The literature is broad but the topic is classical. If you read french, it is notably covered in chapter two of "Psychologie Sociale" by Jacques-Philippe Leyens and Vincent Yzerbyt, but it should be covered in any good (social) psychology textbook. Unless you have a more specific question, this might be the right way to start learning about it.


Chomskian view on grammar The Chomskian view asserts that certain structural components of grammar are innate to all humans. To support the Chomskian view, the observation that we are able to omit certain pronouns in the English language without ever being taught the grammatical rules necessary is used to support the view. However, my question is, what would an example of the above observation be?

Summary:
It's worth noting that all languages have an oral origin so concerning the biological origins of grammar we must look for neurological structures involved in speech processing/production. However, it's worth first clarifying Chomsky's view that there are two levels of innateness: at the level of genetics i.e. biological heredity and at the level of neurological structures i.e. morphology and morphogenesis.
Based on the available evidence, it appears that specific genes and neurological structures that aid language acquisition do exist but these aren't necessarily specific for language.
 Chomsky's view:
Chomsky has historically held firm to the view expressed in 1983 [1]:

QUESTION: Is the role of heredity as important for language as it is
for embryology?
CHOMSKY: I think so. You have to laugh at claims that heredity plays
no significant role in language learning because exactly the same kind
of genetic arguments hold for language learning as hold for
embryological development. I’m very much interested in embryology but
I’ve got just a layman’s knowledge of it. I think that recent work,
primarily in molecular biology, however, is seeking to discover the
ways that genes regulate embryological development. The gene-control
problem is conceptually similar to the problem of accounting for
language growth. In fact, language development really ought to be
called language growth because the language organ grows like any other
body organ.

However, Chomsky also recognised that there was little neurobiological evidence to support this view at the time beyond reasonable hunches:

QUESTION: Is there a special place in the brain and a particular kind
of neurological structure that comprises the language organ?
CHOMSKY: Little enough is known about cognitive systems and their
neurological basis; so caution is necessary in making any direct
claims. But it does seem that the representation and use of language
involve specific neural structures, though their nature is not well
understood.

Chomsky's particular hypotheses:
From the above interview we may derive two hypotheses:

That there might be genes for linguistic ability.
That the development of language may rely on neurological structures that are specific for language.

The first hypothesis is partially validated by research on the FOXP2 gene [3]. In 2001 it was found that in humans the mutation of this gene significantly disrupts speech and language skills.
That said, we must note that FOXP2 has other roles:

...FOXP2 is also expressed in defined regions of other tissues during
embryo development, including the lung, the gut and the heart, as
well as in several tissues of the adult organism.

Given that the heart, gut and lung developed prior to linguistic ability it's more likely that FOXP2 was initially useful for heart and lung function, and was exploited for linguistic ability rather than the other way around. This gene is actually present in other animals. The authors of [3] clarify this point:

the presence of FOXP2 in other animals does not diminish its relevance
for speech and language, but rather represents another example of
recruitment and modification of existing pathways in evolution.

The possibility of specific neurological structures:
Regarding the second hypothesis, this is the subject of ongoing investigation that combines AI research, cognitive science, neuroscience and morphogenesis. How language develops is a very complex and fascinating subject.
In a pioneering robot experiment [2], the linguist and cognitive scientist, Pierre-Yves Oudeyer showed that with basic neural equipment for adaptive holistic vocal imitation, coupling directly motor and perceptual representations in the brain, it was possible to generate spontaneously shared combinatorial systems of
vocalizations in a society of babbling individuals:

...the transition from inarticulated vocalization systems to
human-like speech codes may have been largely due to a modest
biological innovation. Indeed, the model indicates that neuronal
structures that encode a priori and specifically phonemic
organization, as well as typical regularities of speech, do not need
to be innately generated to allow the formation of such speech code.
This is the second contribution of this work: it allows us to
understand how the self-organizing properties of simple neural
structures may have constrained the space of biological vocalization
structures and how speech codes may have been generated and selected
during phylogenesis. These new hypothesis may not have been identified
without the use of computer models and simulations, because the
underlying dynamics are complex and difficult to anticipate through
uniquely verbal reasoning. This illustrates the potential importance
of these new methodological tools in human and biological sciences.

Pierre-Yves' research on robot languages suggests that:

The specific neurological structures that aid acquisition aren't necessarily specific for language.
Cognitive scientists should investigate the development of the vocal tract during language acquisition.

Concerning specific neurological structures, today we know that Broca's area is heavily used for speech production but similar regions are present in other apes that have limited linguistic ability [6]. So it's important to consider the causal influence of Broca's region within cortical networks involved in speech production. In [7] the authors share that:

Using direct cortical surface recordings in neurosurgical patients, we
studied the evolution of activity in cortical neuronal populations, as
well as the Granger causal interactions between them. We found that,
during the cued production of words, a temporal cascade of neural
activity proceeds from sensory representations of words in temporal
cortex to their corresponding articulatory gestures in motor cortex.
Broca’s area mediates this cascade through reciprocal interactions
with temporal and frontal motor regions.

For this reason in the discussion section they infer:

...Broca’s area is not the seat of articulation per se, but rather is
a key node in manipulating and forwarding neural information across
large-scale cortical networks responsible for key components of speech
production.

So far there is a lot of neurological evidence supporting Oudeyer's conjecture that specific neurological structures that aid acquisition aren't necessarily specific for language. As for Oudeyer's second suggestion there's still a lot we don't know. You might be interested in the work of the Max Planck Department for the Neurobiology of Language[4,5].
 References:

Noam Chomsky. Things No Amount of Learning Can Teach. Interviewed by John Gliedman. 1983.
Pierre-Yves Oudeyer. Self-Organization and Complex Dynamical Systems
in the Evolution of Speech. 2013.
Gary F. Marcus and Simon E. Fisher. FOXP2 in focus: what can genes tell us about speech and language? Elsevier. 2003.
Hagoort, P., & Beckmann, C. F. (in press). Key issues and future directions: the neural architecture for language. In P. Hagoort (Ed.), Human Language: From Genes and Brains to Behavior. Cambridge, MA: MIT Press.
Hagoort, P. (in press). Introduction. In P. Hagoort (Ed.), Human Language: From Genes and Brains to Behavior. Cambridge, MA: MIT Press.
Claudio Cantalupo and William D. Hopkins. Asymmetric Broca’s area in great apes. NIH Public Access. 2001.
Adeen Flinker, Anna Korzeniewska, Avgusta Y. Shestyuk, Piotr J. Franaszczuk, Nina F. Dronkers, Robert T. Knight, and Nathan E. Crone. Redefining the role of Broca’s area in speech. PNAS. 2015.


Processing Inverted English Script I was sitting in a restaurant when I realized that it was relatively easy to read this list of a few locations in inverted English script. It made me curious about how it is possible to read this with such ease. It also seems that since these names may be familiar, I might just be engaging in "inverted image" recognition since the normal 'whole image' (e.g. Boston) seems so familiar. Perhaps if these locations were not familiar, it would be slightly harder to process the text.

I was conflicted between posting this in this or in the Linguistics StackExchange but felt that this would be more relevant since there will be multiple perspectives from those interested in neuroscience, psycholinguistics, machine learning and natural-language processing.

A search on the internet seemed to give a lot of instances of the freak-phenomenon of 'mirror writing' and the well-known phenomenon of irrelevance of spelling in comprehension. Furthermore, it is important to notice that this is different from writing of those who are diagnosed with Dyslexia who process language differently (the writing is whole-wise flipped as opposed to individually). However, there seemed to be a dearth of information on this topic in particular. Of course, I am not interested in one-word instances, another example would be like this.

My questions are :-

Are there any good experiments on the phenomenon of processing inverted text ?

Although very little is understood about the neuroscience of language, are there any neurolinguistic perspectives on this phenomenon?

What are the underlying mechanisms hypothesized by the quoted papers in processing such text?

Does there seem to be any evidence of rule-based processing
(e.g. flipping each letter individually)

Are there any good experiments on the phenomenon of processing inverted text?

This is probably the place to start:

Poldrack, Russell A., et al. "The neural basis of visual skill learning: an fMRI study of mirror reading." Cerebral Cortex 8.1 (1998): 1-10.
APA

  What are the underlying mechanisms hypothesized by the quoted papers in processing such text?

"Multiple regions in the occipital
lobe, inferior temporal cortex, superior parietal cortex and
cerebellum were involved in the reading of mirror-reversed
compared to normally oriented text. For novel stimuli, skilled
mirror-reading was associated with decreased activation in the right
superior parietal cortex and posterior occipital regions and
increased activation in the left inferior temporal lobe. These results
suggest that learning to read mirror-reversed text involves a
progression from visuospatial transformation to direct recognition of
transformed letters. Reading practiced, relative to unpracticed,
stimuli was associated with decreased activation in occipital visual
cortices, inferior temporal cortex and superior parietal cortex and
increased activation in occipito-parietal and lateral temporal
regions. By examining skill learning and item-specific repetition
priming in the same task, this study demonstrates that both of these
forms of learning exhibit shifts in the set of neural structures that
contribute to performance."

  Does there seem to be any evidence of rule-based processing?

Yes:

"Mirror-reading skill is letter-specific rather than being a
general visual transformation skill"


Is there any neuroscience research on the emotion of feeling nothing? When people entering anechoic chambers, logically there is a sensation of silence because relatively speaking, the sound levels are much lower compared to some normal baseline
Likewise, when there is emotional numbness there isn't a feeling of emotions nor there is an awareness that there isn't a feeling of emotion and the person will struggle to describe or comprehend emotion adjectives
Also for some people in anesthetics, they shared about what it is like to feel the consciousness is fading
All of these caused me to become curious on what the literature know about the neuroscience such as brain activity when subjects experience these feelings like feeling numb, feeling empty, feeling consciousness is fading, or all at the same time. Unfortunately neither my neuroscience professors are aware of something similar in the literature, nor intense googling on google scholar found any brain activity studies when people felt numb or something stronger

What is the technical name for all these seemly neutral emotions and (lack of) sensations?
Any known famous papers or literature that study the neuroactivity when subjects are experiencing these emotions?

You are talking about 3 different phenomena here (emotional numbness, fading consciousness through medical anaesthesia, and silence within anechoic chambers).  As your title seems to indicate you are actually asking about emotional numbess, I will base my answer on that.
Emotional numbess has been talked about, although not in the same context, in the answers to Can calmness happen during the fight-flight response? and How do certain individuals, like Quang Duc, develop the ability to remain calm when enduring significant nociceptive pain?
Dissociation is the phenomenon involved with emotional numbess as well as physical numbness.

Whilst some define dissociation as a combination of 2 distinct psychological mechanisms (Brown, 2006), the psychobiological mechanism of dissociation is little understood; but, when someone is dissociated from the event, the detachment of conscious awareness from the event can make the person appear very calm.

A person can start to dissociate when a topic of discussion starts which that person is not comfortable with.

Dissociation is a psychological defence mechanism (Cardeña, 1994) which helps the person to get through the situation with as little harm as possible. Think about it like throwing a switch on conscious awareness.

The neuroscience within dissociation is discussed extensively within Krause-Utz, et al. (2017)

Dissociation is a complex heterogeneous phenomenon. It has been defined as a “disruption of and/or discontinuity in the normal, subjective integration of one or more aspects of psychological functioning, including – but not limited to – memory, identity, consciousness, perception, and motor control”. This definition implicates a wide range of psychological symptoms (e.g., depersonalization, derealization, emotional numbing, and memory fragmentations) and somatoform symptoms (e.g., analgesia) [...]
Up to now, the precise neural/neurobiological underpinnings of dissociation remain elusive. Yet, a growing number of neuroimaging studies in DDD, DID, and D-PTSD have implicated dissociative symptoms in altered brain structure and function.

There is a lot of information in the article regarding altered brain structure and function; and reading it will give the full details, but as a snippet:

Aside from functional alterations, several studies reported structural abnormalities in clinical samples with high trait dissociation, although these structural findings are still quite heterogeneous.
In depersonalization disorder, reduced gray matter volumes (GMV) in right thalamus, caudate, and cuneus, and increased GMV in the left dorsomedial PFC and the right somato-sensoric regions were observed . As abovementioned, these areas have been implicated in dissociation.
In DID, reduced volumes in the amygdala and hippocampus and parahippocampus were found, although discrepant findings of normal amygdala and hippocampal volumes compared to healthy controls were also reported. Smaller hippocampal volumes may be related to early life trauma: the hippocampus has a high density of glucocorticoid receptors and is highly sensitive to a heightened release of the stress hormone cortisol—therefore, chronic traumatic stress may lead to cell damage in this area. Smaller hippocampal volumes were also found in healthy individuals with childhood trauma, who did not develop a disorder. Reduced hippocampal volumes in PTSD may therefore stem from a history of trauma rather than specific to the diagnosis. In a recent study, comparing PTSD patients with versus without dissociative subtype, no significant group differences in amygdala, hippocampus, and parahippocampus volumes were observed. Yet, patients with D-PTSD showed increased GMV in right precentral and fusiform gyri and reduced GMV in right inferior temporal gyrus. Severity of depersonalization and derealization was positively correlated with GMV in the right middle frontal gyrus. Another study in PTSD found positive associations between trait dissociation and GMVs in medial/lateral PFC, orbitofrontal, temporal polar, parahippocampal, and inferior parietal cortices—brain regions associated with emotion regulation.

References
Brown, R. J. (2006). Different types of “dissociation” have different psychological mechanisms. Journal of Trauma & Dissociation, 7(4), 7-28. doi: 10.1300/J229v07n04_02
Cardeña, E. (1994) The domain of dissociation. In: Dissociation: Clinical and theoretical aspects, Edited by: Lynn, S. J. and Rhue, J. W. 5–31. New York, NY: Guildford Press.
Krause-Utz, A., Frost, R., Winter, D., & Elzinga, B. M. (2017). Dissociation and alterations in brain function and structure: implications for borderline personality disorder. Current psychiatry reports, 19(1), 6. doi: 10.1007/s11920-017-0757-y pcmcid: PMC5283511


How else can we eliminate wrong underlying beliefs, when even science fails? Source: Why Do Many Reasonable People Doubt Science?, 2015 March, by Joel Achenbach

  [Andrew] Shtulman [of Occidental College] ’s research indicates that as we become scientifically literate, we repress our naive beliefs but never eliminate them entirely. They lurk in our brains, chirping at us as we try to make sense of the world.

This staggered and overwhelmed me: How else can we correct, improve, and refine our lurking, substratal intuitions or instincts that are wrong? I ask NOT about simply  accepting or tolerating facts or science superficially (as insinuated by this excerpt), and remain traumatised.

Footnote: The author has a BA in Politics, and not in science, if this implies anything?

Our memory act as a very powerful database, being able to store a huge load of data. Thing is, that "instinctive data" you learned someday is still there. It might get erased eventually, but as it is "fetched" and used, it gets stronger.

Memory retrieval act akin to a computational weighted-graph navigation, where once you need to remember something, you start navigating in your memories. Memories with greater "weight" or "importance" may be fetched earlier and given a stronger "stamp", i.e., they are more relevant in a given context.

CONSTANTINI, WIKIPEDIA *sigh*:

  Learning and memory are direct consequences of attentional processing: the more attention is directed or devoted toward something, the more likely it is that it will be later learned and remembered.

SURESH, PAVAN KUMAR, AISHWARYA:

  [page 2, §2] Another example which everyone can associate or relate to is remembering an almost forgotten event after a very long time. It so happens that, when we come across a bite of a cookie after decades or smell of a perfume after a long time, we take time to recall what it is about and our association with it.

  ...

  [page 3, §3] [In a face querying context] In the Memory Repeat, the brain repeats the same querying activity until it deduces a relationship between the second image and the fifth image. Once a relationship is establishes, corresponding activities that are chained/outlined to form a bountiful array of events.

  Based upon the data present at the back of the brain, relevant output can be expected. The output might be an association of that image with certain events. It can either be the first time they met or the assignment that any
  had done together or a project/ paper that they had worked upon or classes they had attended, etc.
  It should, however be noted that not all images can yield a positive result. Some associativity (read: data) may have gotten erased as the passage of time.

  A positive result is named as Hit Rate and False Alarm Rate. Hit rate is the positive outcome of a query while False Alarm Rate is the irrelevant or negative outcome of the querying. False alarm rate is the output when an image (or a face) is identical to another image.

If the data is fetched, but never used, it will eventually wear off from the results, but it will only disappear from your brain upon physical memory removal, which takes time.


In a central pattern generator based on reciprocal inhibition, how does one "side" get picked over the other to start out? Consider two neurons, A and B, which reciprocally inhibit each other. If both of the neurons receive input at the same time, it seems to me that no oscillation will occur between the two. Such would occur only if one of the two is initially "favored" over the other. So what I'm wondering is, how does that happen? Is it essentially random?

Noise will ensure that there will not be perfect symmetry and therefore that one has an advantage to fire first.  Whichever one fires first will inhibit the other and ensure that the first one to fire will stay on for however long the dynamics of the pattern generator allow.


How would slowed message over the reflex arc work? Take, for example, a person with average reflexes/a normal reflex arc. The person touches an extremely hot stove and immediately pulls away. Slowing this event down, upon touching the stove, it takes 10 milliseconds to register the pain and then 10 milliseconds to pull away (made up numbers here — not realistic).

If this person's reflex arc was then altered to make the neural message take longer, would the timing be different between (1) afferent neurons and interneurons (e.g., 20ms to feel pain), (2) interneurons and efferent neurons (e.g., 20ms to pull away), or (3) both?

To add on to this: are both paths mentioned above linked together or can they be lengthened/shortened independently?

A prototypical reflex arc just consist of two or three neurons, an afferent (sensory) neuron, possibly one or more interneuron(s), and an efferent (motor) neuron. A reflex arc is a rather direct connection, e.g. just from the sensory organ to the spinal chord and from there to the effector organ – it does not involve processing by the higher parts of the nervous system. To answer your second question: this is one path, consisting of two or more parts (two or more neurons).

It is conceivable that some manipulation would change the reaction time. If we could e.g. somehow replace one of the three neurons with a longer version, the reaction time would somehow grow, and since there are several neurons, their processing time might indeed be manipulated individually. It would not really matter which one of the neurons was manipulated, or if more than one would be manipulated. The total additional reaction time would be the sum of the individual additional reaction times.

To answer your first question: at which of the three neurons the signal were to take longer (»the timing would be different«) would depend upon which one of them was previously manipulated.

There are reflexes that involve more complex neural structure, but nothing like (conscious) bodily feelings/pain.

The withdrawal reflex that you mention is likewise based on receptors in the skin that through their relatively direct linkage with motor neurons can effect a withdrawal reaction without any (consciously) perceived heat or pain.


Are there any agent based cognitive models that are inspired by complex systems studies of ant colonies and economies? I think that certain aspects of ant colony behavior seem almost like economic decision-making in behavior. There are also links between ant colony optimization and features of the brain like selective attention. I was just wondering if any research group has taken up the problems of cognition from the perspectives of economics and/or ant colonies.

It may seem to be mostly analogy on the surface, but the interface of the three seems like a fruitful area to look for new ideas.

Partial answer:
Douglas Hofstadter has written quite a lot about this from a more philosophical approach.
His style isn't for everyone, I think it's introduced well in this chapter ('Ant Fugue').
For more applied work from the same, you might look at Mitchell and Hofstadter's CopyCat model of analogies (described briefly here, as well as on wikipedia).
All this aside, I don't know of any empirical work along the same lines, but I wouldn't rule it out.


Are hot-streaks in athletics real, and if so, is there a known psychological basis? It is common to refer to an athlete who is enjoying a sustained period of success (e.g. a long consecutive game hitting streak in baseball) as being "hot", suggesting that something about their physical or psychological state is different.

However, hitting streaks and other sustained periods of success are bound to happen just by random chance. Therefore, it might be a fallacy to believe that a person is "hot" when really their behavior is expected by random fluctuations in performance.

Is there any research that indicates hot-streaks are real? If so, is there a known psychological basis? (For example, does confidence in one's ability actually improve performance?)

Andrew Gelman has blogged and published about the "hot hand" phenomenon from a statistical perspective. His statistical perspective is probably fairly authoritative, and his psychological perspective, at least in being very inclusive, not implausible. His basic idea is the following:

Previous wins are very unlikely to have no effect on future performance.
Previous wins (or losses) are likely to have some, albeit probably small, effect.

For example, a player's performance could decrease, maybe due to overconfidence
A player's performance could increase, for example, due to increase confidence

Rather than asking if there is any "hot hand" effect at all, the better question is: of what kind is this effect?

In the sense of the latter, the existing studies are actually fairly homogenous: they all argue for a small to marginal effect, on the order of a few percentage points or less. So the idea that the "hot hand" effect is a small and highly variable phenomenon is supported both by a priori reasoning, and by the bulk of the data.

Beyond that, Gilovich, Vallone, and Tversky (1985) have demonstrated that people reliably over detect "hot hands"; we see patterns in near-random variance that aren't really there. Moreover, combining what we know about our perception of the "hot hand", and our statistical knowledge about it, we can establish one more fact: very often, when you think you're observing a "hot hand", you're wrong. This is because the effect size for the "hot hand" appears very small, so small that it is statistically questionable, and if even repeated statistical analyses have trouble establishing its size, we can be sure that the naked eye will not be able to reliably identify it in an individual case.

All this is an example of the debate between null hypothesis testing versus parameter estimation statistics. From the perspective of null hypothesis testing, we consider plausible that the effect might be truly zero, or something else, and zero is our null hypotheses. From the perspective of parameter estimation, we are interested in what the effect actually is, and it being precisely zero is rather unlikely to begin with.

Thus, I believe it justified to say this about the "hot hand" effect:

It exists, in some form or other.
It is likely small, and highly variable (sometimes positive, sometimes close to zero, sometimes even negative).
Whenever you think you see it, you probably don't.


Why do we anchor our happiness to short term situational comparisons rather than large scale events? Why does our happiness seem to be most affected by recent, short term happenings rather than the high level trends of our lives?

For example, a person has begun their life in a very humble or even disadvantaged position: poor education, a lack of parental involvement, and an exposure to drug addiction. This same person, through through their own fortitude manages, to change their life trajectory so that they have a comfortable job, a home in a safe part of town, and many loving friendships. Why then, despite having overcome such odds, are they still likely to be happy or unhappy based on small, localized daily situations, like getting into a disagreement at work or having a friend cancel plans.

To phrase the question a different way, why do large scale personal achievements often have less impact on our moment to moment satisfaction than whatever we're experiencing right now?

Research on well-being has explored happiness from different temporal perspectives.

Much of the literature looks at how people respond to measures of life satisfaction, quality of life, and measures of tendencies to experience positive and negative emotion. These tend to reflect longer term evaluations and emotional experiences. This shows up in for example, the relatively stability that individuals show on such measures. For example Fujita and Diener (2005) examined longitudinal data over 17 years and found substantial correlations in life satisfaction over that period of time.

There are a variety of concepts such as the hedonic treadmill and set point theory which propose that people have a general tendency when it comes to well-being. General daily experiences can lead people to deviate from their set-point, but that with the exception of a few extreme events (e.g., divorce, major trauma, etc.) people tend to return to their set point.

That said, there is another line of research that looks more at the moment to moment affective experience. Such research has often employed experience sampling methods (e.g., Kuppens et al, 2010) and this clearly shows more of what you are talking about: i.e., the way that mood fluctuates in relation to the little daily hassles and pleasures that we experience.

One perspective is that the global assessment and momentary moods serve different functional purposes. Momentary moods help to guide our response in particular situations. For example, a stressful situation may call for increased vigilance or attention. An experience which elicits negative emotions maybe one to avoid. In contrast, global assessments of life satisfaction are much broader and all encompassing and may help to guide us in our broader life plans.

References

Fujita, F., & Diener, E. (2005). Life satisfaction set point: stability and change. Journal of personality and social psychology, 88(1), 158. PDF
Kuppens, P., Oravecz, Z., & Tuerlinckx, F. (2010). Feelings change: accounting for individual differences in the temporal dynamics of affect. Journal of personality and social psychology, 99(6), 1042. PDF


What is a good rough rule of thumb regarding required sample size for questionnaire studies? I need to perform a questionnaire as part of my final project.

What are the quick-and-dirty rules for knowing how many respondents I need to get meaningful results?

Obviously, this question is highly under-specified. The sample size you need depends a lot on the aims of your analysis.

In general, when thinking about sample size requirements, you need to think about power analysis and desired precision of estimation. This in turn requires you to think about your research question and expectations about results (e.g., effect sizes, expected means, and so on).

That said, you asked about a few simple rules of thumbs for questionnaire style research.

These would be my rough rules of thumb:

If you are wanting to do a proper survey study of the population and are aiming to get good  estimates of proportions, then I'd think you'd want at least 1,000 participants in order to get reasonable standard errors. But if you are doing this kind of study, you are going to want to know a lot more about sampling than this question implies.

More likely, you are thinking about rules of thumb for a standard observational psychology study. In these kinds of studies, you are typically measuring several psychology scales perhaps along with some demographics. A typical analysis might involve correlations, regression-type models, and perhaps some reliability analysis and factor analysis to check the scales. In these kinds of studies, I generally think of a sample size of 100 as a reasonable starting point, 200 as good, and 300+ as very good, and of course even bigger samples are better. These rules of thumb are related to the precision with which you are estimating correlations which in turn relate to the precision of predictive models and so on.

For more discussion of rules of thumb, see this question on rules of thumb for regression.

That said, the above are just rough rules of thumb. There are trade-offs between required resources and sample size. More importantly, if you are serious about these things you should analyse your problem in terms of either power analysis or desired precision.


Can bipolar develop in childhood? Is it possible to develop bipolar in childhood? Does the same diagnostic criteria for bipolar in adults apply for children?

Yes but it is referred to as Disruptive Mood Dysregulation Disorder in DSM 5 and is characterized by persistent irritability and frequent episodes of extreme, out-of-control behavior.


Technical term for the displaying of 'bad' traits to seem more likeable What is the technical name for the public display of personal traits that are unproductive or unhealthy as an attempt to make oneself seem more likeable or relatable? (e.g procrastination)

This may not fit exactly the scenario described, but some form of strategic affect display or 'appraisal theory', these relate to social theories of (& displays of) emotion, as oppose personality traits as such, but may be relevant nonetheless.

So for example, you might want to come across as being more aggressive & assertive, or alternately more compassionate & caring, in any given scenario, because you feel that is the appropriate thing to do, or you may gain some advantage from that - even though you may feel otherwise indifferent about whatever it is.

Having said that, the way the question is phrased - whether something is 'productive' or 'unproductive' in a social sense, as oppose to a personal level, is open to interpretation, i.e. if it makes you more 'likeable' then it is socially productive (at least in the short term), regardless of whether it it something that is generally regarded as being a negative trait.

Hope that's relevant.


Does training affect the tactile oblique effect? In the visual sciences it is known that the oblique effect can be reduced by means of training. The oblique effect is observed when testing subjects psychophysically with a grating acuity task (e.g., the BaGa test). Visual acuity is better when horizontal or vertical gratings are tested than when diagonals are used. The performance in discerning diagonal gratings has been shown to improve after training subjects, although performance in the cardinal directions stays better than the oblique stimuli.

The oblique effect has been observed in the tactile sense too (the sense of touch). However, the amount of papers in the scientific literature is quite restricted in the tactile modality. I wasn't able to find evidence in the literature whether training can improve people's performance in tactile diagonal grating tasks.

Can training reduce the oblique effect in the tactile modality, comparable to that observed in visual grating tasks?

Indeed, research on this particular question is somewhat lacking, but what is available suggests that training does improve performance in tactile tests of the oblique effect.

In an article published 1999, Gentaz & Rossetti lament:

  Unfortunately, the effect of practice on the haptic oblique effect has
  not been yet studied.

An indication that this might soon be remedied was noted in  Junker-Tschopp, Gentaz & Viviani (2010):

  We used bars instead of fuzzy stimuli (such as Gabor’s patches)
  because this study is part of a larger project in which we also tested
  learning effects in the haptic modality (blindfolded participants
  explored manually a rod with varying orientations).

It does not look like the results of this "larger project" were ever published.  However, they are reviewed in the book Psychology of Touch and Blindness by Morton A. Heller and Edouard Gentaz (one of the authors of the above mentioned papers) published in 2013 (pp 56-57):

  ... Junker-Tschopp, Gentaz, and Viviani (2010) investigated the extent
  to which visual and haptic perception are penetrable by cognitive
  factors by assessing the effect of learning on the perception of
  orientations.  The "oblique effect" questions the nature of the
  linkages between perception and cognition. ... In the haptic modality,
  the results showed that practice resulted in a general dramatic
  improvement of orientation discriminabilty.   Furthermore, the
  anisotropic bias in orientation perception is actually suppressed by a
  global learning paradigm ...

These results are in line with the idea that the persistence of the oblique effect across modalities indicates that it is situated in higher cognitive processes (it is a top-down effect).  This theory is backed by evidence demonstrating the similarity of the effect across visual and tactile modalities, so the effect of training would be expected to be similar in both.

Unfortunately, not everything is the same about the oblique effect across modalities, and authors note differences such as the role of gravity cues, memory constraints, reference frame, and while training does improve discrimination, it never eliminates the oblique effect, suggesting some bottom-up influence, and hence the potential for differences in results.

In a recent review, Mier (2014) examines the influence of training and feedback on the haptic perception of parallelity, and comes to a more guarded conclusion suggesting a more significant role for bottom-up processes:

  ... Kappers and coworkers (2008) found that the deviations were only
  marginally affected by training and feedback. Without informing their
  participants about their biased performance, they studied the effects
  of visual training (seeing the correct orientations), haptic training
  (feeling the correct orientations) and combined visuo-haptic training
  (seeing and feeling the correct orientations). In addition they
  studied the effect of error feedback on the performance of the
  participants, again under visual, haptic and visual-haptic conditions.
  They showed that the robustness of the deviations persisted even after
  participants received haptic and/or visual feedback and training.
  Haptic or visual training did not significantly decrease the magnitude
  of the deviations, only combining both training modes resulted in a
  small but significant improvement. ... Although providing participants
  with haptic and visual feedback about their errors reduced the
  deviations, performance was still far from being veridical ... As the
  authors state, it might be that extension of the feedback phase would
  eventually lead to more veridical parallel matching.

Compared to the visual realm, where training has failed to eliminate the oblique effect, the effectiveness of training on the tactile oblique effect is unclear.  The first study suggests that training is more effective on the tactile oblique effect, and is capable of entirely eliminating it, while the second study suggests that the tactile effect is less amenable to training than in the visual modality.  Note however, that the second study refers specifically to haptic perception of parallelity, which is a specific sub-case of the oblique effect where exceptionally large oblique effects have been found, and therefore may not be applicable in general.  More research is needed.


fMRI repetition time (TR) and stimulus duration I realized that in many neuroscientific experiments, the duration of the stimulus (say the duration of a grating stimuli displayed to subjects) is considerably shorter than the "TR" (roughly speaking the time between consecutive fMRI data acquisitions of the same cortical location) - an example would be a stimulus duration of 500 ms and a TR of 1.5 seconds.

My question: Does this not mean that some measurements have a very low signal-to-noise ratio, or can this approach be justified by the BOLD responses relatively long duration?

(f)MRI does not have good temporal resolution. If that is needed something like EEG or MEG is used, but the latter have low spatial resolution (hard inverse problem).
Also note that the low temporal resolution of fMRI is due to BOLD response time (i.e. it's not just the case  that the current fMRI technology sucks)

  fMRI’s temporal resolution is limited by hemodynamic response time; typically the BOLD response has a width of ~3s and a peak occurring ~5–6s after the onset of a brief neural stimulus. This is much slower than the underlying neural processes, and temporal information is thereby heavily blurred.

Without getting into the specifics of the experiment (what's that you're actually trying to measure) it's impossible to say whether fMRI (=BOLD) would be inappropriate.

Also noise and blur are not the same issue; loot at some illustrations and it should be obvious without getting into math.


How is tone volume encoded? I am wondering whether increasing the volume would result in (a) a neuron that was already firing to now increase its spike rate, (b) a different group of neurons to add their activity to the population total, (c) a different group of neurons, coding for the new volume, to become active while the first group of neurons silences, or (d) some combination of the above. In particular, I am curious about the subcortical portion of the auditory pathway.

There are quite a few stations between cochlea and the brain and I will focus on the auditory nerve. That said, your theories (a) and (b) are both correct, and therefore (d) applies as well.

(a) Neurons in the auditory nerve increase their firing rate when sound level is increased (Heil et al, 2011). This can be regarded as the primary mechanism for encoding sound level.

(b) Increased sound levels are accompanied by a larger area in the cochlea being activated due to the low-frequency tail (Kiang & Moxon, 1974). Hence, more neurons start firing at higher sound levels when the tone frequency is the same. Although this may add in the perceived sound level, it is likely of less importance than (a), as it is basically a reflection of the mechanical properties of the basilar membrane in the cochlea and primarily reduces frequency resolution.

(c) There are no neurons ever identified that are dedicated to sound level encoding. Instead, auditory nerve fibers encode sound frequency (according to the place-frequency map of the cochlea) and they encode sound intensity via their firing rate.

(d) Hence, since both (a) and (b) are correct, your hypothesis (d) holds, as it is a combination of the above.

One can safely assume these intensity-coding mechanisms hold up in the responses of neurons in the next station - the cochlear nucleus. However, the higher up you go in the auditory system, the less likely a 1:1 relationship as found in the far periphery applies.

References
 - Heil et al., J Neurosci 2011; 31(43): 15424-37
 - Kiang & Moxon, JASA 1954; 55(3): 620-30


What kind of cognitive psych journals are receptive to clinicians without any publications? A good friend of mine is a clinical psychologist. She has been in practice for more then 25 years and has provided psychological help to people for a variety of issues.

One of her specialities is ADHD. She has created what cognitive psychologists call a "process model"  (ie flow chart model; see Cognitive Psychology by Goldstein for definition) for how ADHD could work as well as solutions for how to correct it based on her expect experience with her patients. She thus helps people successfully adapt to having the disorder by training them using her model.

All she has at the moment is a model, but she feels very confident publishing this model could help other since it has been successful in her clinical work.

She is capable of organizing these ideas into arguments suitable for academic discourse and likely could also find peers to help edit her work. But she must find a journal that would be interested in publishing her model.

I myself do not know much about publishing in psychology and am more familiar with biology and physics. However, from talking to my physicist friends, I have learned there are a lot of changes going on in how articles are published and correspondingly what opportunities are available. She has not considered publishing until recently (last few years) and is trying to get a better sense of what avenues would be appropriate / sensible.

My Question:

What kind of journal might be suitable for my friend to attempt to submit to?

Note:

The main purpose of this question is to (1) get more information about trends in how publishing works in psychology journals and (2) to get information specifically about what cognitive psychology journals (specifically those who accept process models) look for in accepting papers. Obviously, it will vary a lot but I just want some starting food for thought.  I am not primarily looking for advice but for general information. Any advice is welcome however. I just provided this note in an attempt to ensure it is on topic and not too broad so its useful for others too.

(note: quotes are from useful comments on the question)

  "I think clinical psychology journals would be her best option either way. Without new data, comments from others about reviewing existing models and data are even more critical. Unfairly, scientists often don't like new theories or models being proposed by people without a scientific track record, so I would recommend a journal with double-blind review, so her ideas can be evaluated on their merits and not on her name recognition." -- DanM

With regard to a paper on ADHD in particular,

  "One can generally advance a new model based on a review of the literature. In her manuscript, she might (1) review the relevant ADHD literature, (2) review relevant ADHD models, and (3) propose a new model that is based on (1) and overcomes limitations of the models in (2). She can also suggest how the model might be employed in clinical practice, and use anecdotal evidence mixed with scientific evidence from the literature to back this up. Without some kind of clinical trial(s) (as an evidence base), it's difficult to talk about the efficacy/effectiveness of her therapy." -- mrt

If she writes the kind of article requiring evidence, then her evidence should be something along the lines of this:

  "Regarding evidence base: a key issue is whether she will be reporting the results of systematic data collection or anectodal observations. If she has consistent clinical notes, she could do a systematic retroactive data analysis (as in systematic chart reviews in medical research). More generally, clinical psychology journals (esp. those focusing on pediatric or developmental psychopathology or neuropsychology) will probably be more receptive to this kind of work than cognitive psychology journals." -- DanM