# Question
Title: Are Sex Offender Treatment Programmes (SOTPs) effective?
## Background to my question on SOTPs

NOMS is the UKs National Offender Management Service, which is now called Her Majesty’s Prison and Probation Service.

If you look at the UKs official website on Offender Behaviour Progammes (OBPs) run by Her Majesty’s Ministry of Justice, it states

> There is growing international evidence that the type of cognitive-behavioural techniques that NOMS accredited programmes apply are the most effective in reducing offending behaviour; evidence Fact Sheets are available from Interventions Unit.

Trying to find these fact sheets is difficult, but a document titled *Suitability for Accredited Interventions* (NOMS, 2010) has the following on page 5.

> A number of offenders are either diagnosed with Personality Disorder or present complex needs linked to their risk. The degree of complexity may prevent them from engaging fully with a shorter programme or may make shorter interventions inadequate. In this instance, a referral should be considered for a Democratic Therapeutic Community (DTC).
>
> Participation in a DTC can occur at any point during the sentence, depending on the needs of the offender. Some will benefit from completing shorter programmes, such as ETS/TSP first to support responsivity and engagement in the DTC. Other offenders may find the therapeutic community approach can prepare and support participation in future high-intensity offence-focussed interventions, if applicable. DTCs currently exist in the Category B and C closed prison estate.
>
> Further information on DTCs can be found at Appendix D.

Appendix B (Page 45) covers all the tyes of SOTP in detail

Appendix D (Page 65) states

> **Democratic Therapeutic Communities (DTCs) (Custody)**
>
> Democratic TCs provide a living-learning intervention for offenders whose primary criminogenic risk factors need to be targeted whilst simultaneously addressing psychological and emotional disturbance.

This is followed by details of the risk assessments required, including a

> Sexual Offences Attitude Questionnaire (Hogue & OBPU) (for male sex offenders only)

and the questionnaire

> can be used independent of whether the victim or victims were male or female, adult or child. (Hogue, 1994)

## My Question

Apart from what I mentioned above, I found the following:

* a study (Wakeling, et al., 2007) covering UK SOTPs by **evaluating participants’ experiences** using both qualitative and quantitative methods.
The authors state that

> SOTP staff from the establishments conducted the interviews, most of whom were involved within treatment delivery. Participants’ responses may therefore have been more positive than they would have been if an independent party had interviewed them.
* Beech, et. al. (1998) **again used offender questionnaires**!

> Two approaches were used to evaluate treatment impact. The first approach examined the extent to which treated child abusers showed statistically significant changes in their levels of denial, pro-offending attitudes, and social competency/acceptance of accountability. Using this approach it was found that both shorter (80 hours) and longer treatment groups (160 hours) were effective in producing statistically significant reductions in these areas
> The second, and more sophisticated, analysis considered to what extent the child abusers had, by the end of treatment, a ‘treated’ profile.

## Are there any studies which evaluated effectiveness using data on reoffending rates?

A study on Californian programmes (Marques, et al. 2005) states that:

> The study was a randomized clinical trial that compared the reoffense rates of offenders treated in an inpatient relapse prevention (RP) program with the rates of offenders in two (untreated) prison control groups. No significant differences were found among the three groups in their rates of sexual or violent reoffending over an 8-year follow-up period.

## Has there been any further evaluation, and is this the same with the UK SOTPs and the rest of the US?

## References

Beech, A. et al. (1998). *Evaluation of a National Prison-based Treatment Program for Sexual Offenders in England and Wales*. Journal of Interpersonal Violence 18(7), 744—59
DOI: 10.1177/0886260503253236

Hogue, T. (1994). Sexual offence information questionnaire: assessment of sexual offenders' perceptions of responsibility, empathy and control. In: *Rights and Risks: the application of forensic psychology*. British Psychological Society, Leicester, pp. 68-75
**Abstract available only - PDF RESTRICTED to Repository Staff, University of Lincoln**
http://eprints.lincoln.ac.uk/2844/

Marques, J.K. et al. (2005) Effects of a Relapse Prevention Program on Sexual Recidivism: Final Results From California’s Sex Offender Treatment and Evaluation Project (SOTEP). *Sexual Abuse: A Journal of Research and Treatment* 17(1), 79–107
DOI: 10.1007/s11194-005-1212-x

NOMS. (2010). *Suitability for Accredited Interventions* \[Word Document\]
Available at: https://www.gov.uk/government/uploads/system/uploads/attachment\_data/file/259175/annex-sotp-programmes.doc

Wakeling, H. et al. (2007) Sexual offenders' treatment experience: A qualitative and quantitative investigation. *Journal of Sexual Aggression* 11(2), 171—186
DOI: 10.1080/13552600412331321323

# Answer
## Short answer

Sex offending is high in the public consciousness, but people should know that the treatments offenders receive in prisons and secure hospitals lack evidence of efficacy (Ho, 2015), and ineffective treatment of sex offenders fails victims as a recent report (Mews, Bella & Purver, 2017) highlights worse risk rather than lower after treatment.

## Long Answer

The recent widespread publicity surrounding well known public figures who have been accused or convicted of sex offensesexamples: \[1\]\[2\]\[3\] has indelibly etched sex offending into the UK public’s consciousness. Sex offending is not a new phenomenon. However, what is new is the revelation of these offenders’ profiles, their positions of influence, and the sheer number and duration of these offenses, which were perpetrated and undetected for so long. Even though many high profile cases have been classed as “historical offenses” many victims still experience consequences (Ho, 2015).

The Sex Offender Treatment Programme (SOTP) is the standard psychological talking therapy used in prisons and secure psychiatric hospitals in England and Wales since 1991. Mostly in groups, offenders follow a syllabus (Ho, 2015) that includes discussions about healthy relationships, triggers for sex offending, thinking styles, effects on victims, emotional management, and intimacy skills. The “core” group meets for six months (86 group sessions) and the “extended” group for an additional four months. After these sessions, if offenders have kept out of trouble they stand a better chance of early release from prison. Certainly, parole board hearings place some weight on offenders having completed “treatment” when considering whether to release them on licence.

In response to David Ho's review paper, Dr. Jamie Walton, employed in HM Prison Service and a current Treatment Manager of the Core Sex Offender Treatment Programme (SOTP) within a regional Treatment Management team at the time, said:

> We believe that Ho’s conclusion is premature. Claiming that treatment is ineffective in the absence of consistent high quality evidence to support such a claim does not accurately convey the state of affairs in the field. Only through increasing the rigor of studies in the field together with efforts to identify the influence of residual bias on outcomes of interest can progress occur.
> (Source: BMJ Rapid Responses)

No evidence from academic or policy research has shown that the treatment programme significantly reduces sexual reoffending (Dennis, et al. 2012; Lösel & Schmucker. 2005; Ho & Ross. 2012). Also, there was a damning report put together by HM Ministry of Justice **Analytical Services** (Mews, Bella & Purver, 2017), which highlighted that sexual reoffending rates are 2% higher after SOTP treatment and Child image reoffending rates are 1.6% higher indicating worse risk rather than lower after treatment:

> The **binary reoffending rates**23 over an average 8.2 year follow up period were mostly similar between the matched treatment and comparison groups (see Table A.8, parsimonious model24). The only statistically significant differences emerged on the following outcomes:25
>
> * Sexual reoffending:26 the reoffending rate for the treatment group was 2.0pp higher than the matched comparison group (10.0% vs. 8.0%);
> * Child image reoffending: the reoffending rate for the treatment group was 1.6pp higher (4.4% vs. 2.9%).
>
> ---
>
> 23 Proportion of offenders who committed at least one reoffence during the follow-up period
>  24 See Annex C for a description of the methods used to develop the parsimonious and less parsimonious models.
>  25 Propensity score matching was performed in Stata with *psmatch2* (Leuven and Sianesi, 2003). Although the statistical significance calculations in *psmatch2* do not take account of the fact that the propensity scores themselves are estimated, very similar results were obtained using 95% CIs generated by bootstrapping, which does take account of propensity score estimation.
> 26 Unless otherwise stated, the sexual reoffending measure used in this report includes all sexual offences except breaches

> The frequency of reoffending27 outcomes were also mostly equivalent between the matched groups (see Table A.9, parsimonious model), with statistically significant differences emerging only for:
>
> * Sexual reoffending: the matched treatment group had 0.15 more reoffences per offender than the matched comparison group (0.59 vs. 0.45).
> * Adult other: the matched treatment group had 0.02 more reoffences per offender than the matched comparison group (0.04 vs. 0.02).
> * Non-sexual: the matched treatment group had 0.27 fewer reoffences per offender than the matched comparison group (0.98 vs. 1.25).
> * Non-sexual non-violent: the matched treatment group had 0.27 fewer reoffences per offender than the matched comparison group (0.92 vs. 1.19). This seems to ‘drive’ the above difference in the overall non-sexual frequency of reoffending.
>
> ---
>
> 27 The number of reoffences per offender during the follow-up period.

**More can be found in:**

Forde, R. A. (2017). *Bad Psychology: How Forensic Psychology Left Science Behind*. Jessica Kingsley Publishers.

## References

Dennis, J. A. & Khan, O., Ferriter, M., Huband, N., Powney, M. J. & Duggan, C. (2012). Psychological interventions for adults who have sexually offended or are at risk of offending. *Cochrane Database of Systematic Reviews* 12(1).
DOI: 10.1002/14651858.CD007507.pub2

Ho, D. K. (2015). Ineffective treatment of sex offenders fails victims. *British Medical Journal* 350.
DOI: 10.1136/bmj.h199 PMID: 25627560

Ho, D. K. & Ross, C. C. Cognitive behaviour therapy for sex offenders: too good to be true? *Criminal Behaviour and Mental Health* 22(1), 1—6.
DOI: 10.1002/cbm.1818

Lösel, F. & Schmucker, M. (2005).The effectiveness of treatment for sexual offenders: a comprehensive meta-analysis. *Journal of Experimental Criminology* 1(1), 117—46.
DOI: 10.1007/s11292-004-6466-7

Mews, A. Bella, L. D. & Purver, M. (2017). Impact evaluation of the prison-based Core Sex Offender Treatment Programme \[Free PDF\]
Available at: https://www.gov.uk/government/uploads/system/uploads/attachment\_data/file/623877/sotp-report-print.pdf
> 13 votes

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Tags: criminology
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# Question
Title: Brain areas active while learning hierarchical structure of a problem
There are multiple examples in the machine learning literature of trying to learn the hierarchical structure of a reinforcement learning problem, however have there been any papers tying this learning to neurological activity in the brain?

The type of evidence I would like some indication of a neural substrate indicating some type of activity when learning a hierarchical structure is necessary to solve a problem vs. when a simple problem is attempted.

# Answer
> 1 votes
According to "Frontal Cortex and the Discovery of Abstract Action Rules" by David Badre, Andrew S. Kayser, and MarkD'Esposito:

> ... the rostro-caudal axis of frontal cortex support rule learning at higher levels of abstraction. Moreover, these results indicate that when humans confront new rule learning problems, this rostro-caudal division of labor supports the search for relationships between context and action at multiple levels of abstraction simultaneously.

They found this by contrasting fMRI signals collected while the subject performed two tasks, one requiring a hierarchical, abstract rule and one requiring a flat, basic mapping.

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Tags: reference-request, cognitive-neuroscience, reinforcement-learning
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# Question
Title: Can you get addicted from using topical or local anaesthetics to ease pain?
I've been wondering if there was such a thing as developing some kind of physical or psychological dependence on things that relieve pain. While we often hear about opioid addiction, which is primarily physical, I wonder if someone could psychologically be hooked on using something like lidocaine to numb every bruise or injury they get, just to numb the pain.

I did hear that cocaine was once used as an anaesthetic, but it was also physically addicting. This makes me wonder if physical withdrawal and hunger cravings are similar.

# Answer
**Short answer**
Basing an answer strictly on the DSM-V criteria, local anesthetics *may*, purely hypothetically, be associated with a mild form of addiction. But realistically, I think it is unlikely that a person (ab)using a topical anesthetic will ever be medically diagnosed as having a substance abuse disorder.

**Background**
I think the question hinges on the definition of \[drug\] **addiction**. The APA addresses **addiction in DSM-V** by the following criteria (entered in shortened form for brevity):

> A minimum of 2-3 criteria is required for a **mild substance use disorder** diagnosis, while 4-5 is moderate, and 6-7 is severe \[...\]
>
> 1. Taking the opioid in larger amounts and for longer than intended
> 2. Wanting to cut down or quit but not being able to do it
> 3. Spending a lot of time obtaining the opioid
> 4. Craving or a strong desire to use opioids
> 5. Repeatedly unable to carry out major obligations at work, school, or home \[...\]
> 6. Continued use despite \[...\] social or interpersonal problems \[...\]
> 7. Stopping or reducing important social, occupational, or recreational activities \[...\]
> 8. Recurrent use of opioids in physically hazardous situations
> 9. Consistent use of opioids despite \[...\] physical or psychological difficulties \[...\]
> 10. \[Development of t\]olerance \[...\]
> 11. \[Development of w\]ithdrawal \[symptoms\]

In contrast to opiates, **lidocaine has no rewarding or addictive properties**. As a result, lidocaine can be used systemically and on a long-term basis for the treatment of chronic pain (Yousefshahi *et al*., 2017). In fact, lidocaine, has equally effective anelgesic effects in people addicted to opioids as in normal controls (Hashemian *et al*., 2013). Because lidocaine is a local anesthetic without central effects, and taken together with above findings, we can safely rule out the occurrence all of the criteria except, perhaps, the first three. Those first three may be, at least hypothetically, possible when topical or systemic application relieves some sort of untolerable pain. Given that meeting 3 criteria meets the definition of a mild substance abuse disorder (mild addiction), I wouldn't rule addiction to topical anesthetics out completely. It does seem unlikely, though.

Cocaine has strong addicitve effects, because of it's pronounced effects in the central nervous system - it is associated with strong feelings of reward and euphoria. It rapidly induces tolerance as well as dependence; a school book example of a substance of abuse. Lidocaine is a cocaine derivative that still exhibits its anelgesic properties, without its psychoactive component (Small, 2009).

<sub>**References**
**-** Hashemian *et al*., *J Emerg Trauma Shock* (2014); **7**(4): 301–4
**-** Small, *Subst Use Misuse* (2009); **44**(13): 1888-98
**-** Yousefshahi *et al*., *Anesth Pain Med* (2017); **7**(3): e44732</sub>
> 2 votes

# Answer
> I've been wondering if there was such a thing as developing some kind of physical or psychological dependence on things that relieve pain.

Yes. However:

You need to be careful about your use of the word pain: opioids are analgesics, they relieve the subjective experience of pain. They're addictive.

Lignocaine is a local anaesthetic: it prevents *nociception* or the sensory input that indicates the presence of a noxious stimulus. This in turn renders the relief of any pain unnecessary.

More broadly, however, I was going to suggest that people can become addicted to unpleasant things, not because the unpleasant this is pleasant per se, but because the removal of said unpleasantness is relieving.

A little tangential, but may be worth a read: Are nonpharmacological induced rewards related to anhedonia? A study among skydivers

> While we often hear about opioid addiction, which is primarily physical,

This is where you've lost me. While opioid dependency is definitely characterised by physical features e.g. withdrawal syndrome, I think it's very inaccurate to consider it purely a "physical" dependency. If this were the case, then following a prolonged period of abstinence, there would be no concern of relapse -- the once dependent individual has no "physical addiction" to opioids to speak of.

If you would like to know the difference between "physical" dependency to opioids and "physical and psychological" dependency to opioids, I would suggest the following treatment schedule:

1. Take the OTC medication loperamide, which is an opioid agonist that cannot cross the BBB.
2. 1 week washout
3. Take heroin every 8 hours for two weeks
4. 1 week washout
5. Report back if you noticed a difference between heroin and loperamide.

> I wonder if someone could psychologically be hooked on using something like Lidocaine to numb every bruise or injury they get just to numb the pain.

Yes, but not for the reasons you are thinking.

Local anaesthetics act locally, and are the functional equivalent of a reversible lesion to the nerves they are acting on. Anything that an individual finds pleasant can become "addicting", but with respect to lignocaine, it's prudent to note that if it were addictive, it would have nothing to do with any action centrally.

> I did hear that cocaine was once used as an anaesthetic, but it was also physically addicting.

Cocaine is still used in ENT surgery, as it is an highly effective vasoconstricting agent.

Its addictive properties, however, are largely thought to be limited to the "psychological" space. Yes, I state that in full appreciation for the above regarding physical. This is not to say that an individual does not have "physical symptoms" e.g. tiredness, but that these symptoms have a locus somewhere in the brain.

> This makes me wonder if physical withdrawal and hunger cravings are similar.

One concept in neuroscience/neuropsychology is the *somatic marker hypothesis* by Dimasio, which proposes that our behaviours/decisions are effectively guided by somatic, or physical sensations that are strongly linked to our emotions.

Thus, the body's need for food would instantiate a physiological state of discomfort that drives us behaviourally to seek food.

Likewise, the body's need for more IV heroin, would evince its own set of "somatic markers" likely to guide one's own behaviour towards the acquisition of more intravenous heroin.

See below:

> The somatic marker hypothesis: A neural theory of economic decision
>
> Modern economic theory ignores the influence of emotions on decision-making. Emerging neuroscience evidence suggests that sound and rational decision making, in fact, depends on prior accurate emotional processing. The somatic marker hypothesis provides a systems-level neuroanatomical and cognitive framework for decision-making and its influence by emotion. The key idea of this hypothesis is that decision-making is a process that is influenced by marker signals that arise in bioregulatory processes, including those that express themselves in emotions and feelings. This influence can occur at multiple levels of operation, some of which occur consciously, and some of which occur non-consciously. Here we review studies that confirm various predictions from the hypothesis, and propose a neural model for economic decision, in which emotions are a major factor in the interaction between environmental conditions and human decision processes, with these emotional systems providing valuable implicit or explicit knowledge for making fast and advantageous decisions.
> 1 votes

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Tags: neuroscience, behaviorism, psychopharmacology, addiction
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# Question
Title: Understanding fear as a response in classical conditioning
I have difficulties to understand fear as a response to a stimuli. In my view fear occurs as a anticipation of a possible threat in the (nearby) future. Fear prepares the organism so that it can react faster to the threat (eg. fight or flight response). Thus, the order of the stimulus (threat) and the response (fear) is changed ("fear -\> threat" instead of "threat -\> fear"). So I would describe this connection as "preparation -\> stimulus" instead of "stimulus -\> response".

I would argue that stimuli which cause fear (eg. loud noise) are predictors of a threat. Thus for the reaction "loud noise -\> fear" we have a second order conditioning since the association "loud noise -\> threat" was created before.

In a similar way I would describe other fear conditioning processes. When for example a student develops a test anxiety, after multiple exams a student often experience (extremely) negative responds which he / she experience as a threat. Thus he / she learns the connection "exam -\> threat" and responds with fear at upcoming exams in order to prepare herself / himself for the anticipated threat.

*My Questions:*

* Is this a valid description of fear conditioning?
* Is it in general possible that in classical conditioning the order "stimulus -\> response" is changed to "preparation behavior -\> stimulus"?

# Answer
## Short answer

You are almost there. The 5F (fright/flight/fight/freeze/fawn) response to threats is an unconscious reflex which **in brief** follows as **Threat → Fear → Response**.

A lot of people cannot understand the "fawn" response and https://drarielleschwartz.com/the-fawn-response-in-complex-ptsd-dr-arielle-schwartz gives a good write-up on it.

With classical conditioning, this occurs when an unconditioned response (an unlearned reflex response e.g. salivation) is turned into a conditioned response (a learned reflex response) (Source). Therefore a conditioned response of fear would be consciously created initially through **stimulus → fear → learned threat**, which after successful conditioning will change to the normal unconscious 5F response.

## Long answer

### The 5F (fright/flight/fight/freeze/fawn) response to threats

As you can see from the info-graphic below, The 5F (fright/flight/fight/freeze/fawn response) to threats, is initiated from **Threat → Brain Receiving Signals → Brain Reacts (Fright) → Cortisol and Adrenaline is released → Physical Reactions occur (see quote below) from the release of hormones → Bodily response (Fight, Flight, Freeze or Fawn)**

( (Source: Wikipedia)

> The reaction begins in the amygdala, which triggers a neural response in the hypothalamus. The initial reaction is followed by activation of the pituitary gland and secretion of the hormone ACTH. The adrenal gland is activated almost simultaneously, via the sympathetic nervous system, and releases the hormone epinephrine. The release of chemical messengers results in the production of the hormone cortisol, which increases blood pressure, blood sugar, and suppresses the immune system. The initial response and subsequent reactions are triggered in an effort to create a boost of energy. This boost of energy is activated by epinephrine binding to liver cells and the subsequent production of glucose. Additionally, the circulation of cortisol functions to turn fatty acids into available energy, which prepares muscles throughout the body for response. Catecholamine hormones, such as adrenaline (epinephrine) or noradrenaline (norepinephrine), facilitate immediate physical reactions associated with a preparation for violent muscular action and:

* Acceleration of heart and lung action
* Paling or flushing, or alternating between both
* Inhibition of stomach and upper-intestinal action to the point where digestion slows down or stops
* General effect on the sphincters of the body
* Constriction of blood vessels in many parts of the body
* Liberation of metabolic energy sources (particularly fat and glycogen) for muscular action
* Dilation of blood vessels for muscles
* Inhibition of the lacrimal gland (responsible for tear production) and salivation
* Dilation of pupil (mydriasis)
* Relaxation of bladder
* Inhibition of erection
* Auditory exclusion (loss of hearing)
* Tunnel vision (loss of peripheral vision)
* Disinhibition of spinal reflexes
* Shaking.

**All of this occurs without conscious thought** as analysis of the signal doesn't takes place until after action has been taken.

### Classical Conditioning

With classical conditioning (also known as **Pavlovian** or **respondent conditioning**), this occurs when an unconditioned response (an unlearned reflex response e.g. salivation) is turned into a conditioned response (a learned reflex response) after

> a conditioned stimulus (CS) is paired with an unconditioned stimulus (US). Usually, the conditioned stimulus is a neutral stimulus (e.g., the sound of a tuning fork), the unconditioned stimulus is biologically potent (e.g., the taste of food) and the unconditioned response (UR) to the unconditioned stimulus is an unlearned reflex response (e.g., salivation).
> (Source)

A conditioned response of fear would initially be consciously created through **stimulus → unpleasant sensation** maybe this will have to occur 2 - 3 times or more before the next stage which is **learnt fear → learned threat**, which after successful conditioning will change to the normal unconscious 5F response.
> 1 votes

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Tags: learning, behaviorism, conditioning, fear
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title: What is the most readable screen font?

text:
# Question
Title: What is the most readable screen font?
Fonts (i.e. letters) that facilitate reading in print don't always read well on a computer screen. New fonts such as Verdana have been developed especially for screen presentation of text.

There is some research that compares the readability of those fonts that are available across most operating systems: Times, Arial, Helvetica and Arial. For example, this study found that Times New Roman can be read faster than Verdana.

But there are thousands of other fonts, and maybe one font not commonly shipped with any OS would be even more easily readable, or at smaller sizes. Of course no empirical research can include all fonts that exist, but maybe there is some research that goes beyond the common websafe fonts.

**Have there been attempts to create the most readable screen font that were supported by empirical tests? Or is there empirical research into screen font readability including non-websafe fonts?**

# Answer
## For print (Generally)

> In his book Cashvertising, Drew Eric Whitman cites a 1986 study of fonts (printed on paper) that found only 12 percent of participants effectively comprehended a paragraph set in sans-serif type versus 67 percent who were given a version set in serif typeface ...
>
> In a test of three different fonts, two serifs (Garamond and Times New Roman) and one sans serif (Helvetica), he found
>
> * 66 percent were able to comprehend Garamond;
> * 31.5 percent Times New Roman, and
> * 12.5 percent Helvetica
> (out of a total of 1,010,000 people surveyed).
>
> (Source)

## On screen (Generally)

> Several observations can be made regarding the examined font types. First, no significant differences in reading efficiency were detected between the font types at any size. There were, however, significant differences in reading time. Generally, Times and Arial were read faster than Courier, Schoolbook, and Georgia. Fonts at the 12-point size were read faster than fonts at the 10-point size. In addition, a font type x size interaction was found for the perception of font legibility. In general, however, Arial, Courier, and Georgia were perceived as the most legible.
>
> For font attractiveness, Georgia was perceived as being more attractive than Arial, Courier, and Comic, while Times was perceived as more attractive than Courier. (Bernard, et al. 2002)

## But it is not that simple

Dyslexia sufferers can have different requirements. Most of the recommendations come from associations for people with dyslexia and they agree in using sans-serif fonts. The British Dyslexia Association recommends

* Use Arial, Comic Sans or, as alternatives to these, Verdana, Tahoma, Century Gothic, and Trebuchet
* Most users prefer dark print on a pale background but colour preferences vary
* Avoid green and red/pink as these are difficult for colour-blind individuals.
(British Dyslexia Association, 2012).

## Also

WebAIM also has articles and resources for those with accessibility in mind

## References

Bernard, M. et al. (2002). *A Comparison of Popular Online Fonts: Which Size and Type is Best?* \[Online\]
Available at: **Wichita State University Software Usability and Research Laboratory**
http://usabilitynews.org/a-comparison-of-popular-online-fonts-which-size-and-type-is-best

British Dyslexia Association. (2012). *Dyslexia style guide* \[Online\]
Available at: http://www.bdadyslexia.org.uk/common/ckeditor/filemanager/userfiles/About\_Us/policies/Dyslexia\_Style\_Guide.pdf
> 1 votes

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Tags: perception
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# Question
Title: In TD learning, is the weight function used as a linear filter?
In the Temporal difference learning algorithm (TD-learning), an agent seeks to predict the total value of future rewards that will be received during the current trial. The agent updates the prediction as the trial progresses, based on conditioned stimuli (CS) that have been seen so far. Specifically, the prediction is calculated as a weighted sum of the intensities of past CS presentation. At time $t$, the prediction is calculated as

$$v(t) = \sum\_{z=0}^t w(z)u(t-z)$$

where $v(t)$ is the prediction at time $t$, $u(t)$ is the CS intensity at time $t$, and $w$ is an array of weights.

My question is: why are we summing the terms $w(z)u(t-z)$, rather than $w(z)u(z)$, i.e. why isn't each weight associated with the CS strength at a particular time?

\[Thanks to user honi's reply, I subsequently understood that each element of the weight array is associated with an elapsed time since seeing the CS. For example, $w(3)$ is the weight given to the CS strength experienced three units of time ago.\]

---

\[Original phrasing of the question: I am reading Theoretical Neuroscience by Dayan and Abbot, and I am confused by the use of $w(t)$ in equations (9.6) and (9.7). In the former, it is a window function (linear filter) and in the latter it is the weight function. Is this (a) an unfortunate use of the same name for two different things, or (b) is the weight function really used as a linear filter to calculate $v(t)$?\]

# Answer
> 2 votes
They are the same in the two equations. See equation 9.3: v = w\*u. w and u are bolded in that equation to indicate that they are vectors. In equation 9.3, they are vectors of simultaneously presented stimuli, but you can apply the same equation if u is a vector of a single stimulus over time and w are the weights of each time step of that stimulus. Indeed, a linear filter is simply a way to weight different time steps of a time-varying input. Note that v in equation 9.3 is a single value, whereas v in equation 9.6 is a function of t, i.e. it has a different value at each time point depending on what part of u is currently occurring.

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Tags: neuroscience, theoretical-neuroscience, computational-modeling
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title: Synesthesia hearing to see

text:
# Question
Title: Synesthesia hearing to see
Can a synesthetic person, also known as a synaesthete, see sounds even when that person is actually blind? If so how does the brain interpret a picture without a vision?

# Answer
In order for your 2 questions to be answered I have taken each question in turn.

## Can a synaesthete see sounds even when that person is actually blind?

According to Steven & Blakemore (2004), there seems to be 2 forms of visual synaesthesia which blind people can experience. That is **Coloured-Braille synaesthesia**, and **Coloured-hearing synaesthesia for letters, numbers, and words (including time-related words)** This is also known as Chromesthesia (see also this Wikipedia Article). All quotes below are from Steven & Blakemore's study article, and there is one point of note with the study.

> The synaesthesia described by our subjects is most likely idiopathic (ie of early onset, as opposed to acquired after blindness) because all of them report having had synaesthesia for as long as they can remember (ie from prior to the onset of blindness). Furthermore, three of the six subjects have one or more first-degree relatives who are sighted and have synaesthesia (suggesting a genetic aetiology for the phenomenon)

I haven't come across any study where people blind from birth can experience synaesthesia, yet it doesn't mean it cannot happen. The question then of course would be how the colours could be relayed to someone studying the case as the person blind from birth would not have any colour references to go by.

### Coloured-Braille synaesthesia

This is where the blind person sees colours whilst reading Braile.

> One subject, JF, reports experiencing coloured Braille. For JF, the tactile sensation of each Braille character immediately evokes a synaesthetic impression of an array of tiny coloured dots, "like an LED display", corresponding to the Braille character. However, he does not see colours when he feels other textures or objects with his fingers, nor when he touches dots arranged in shapes or spatial arrangements not related to Braille.

### Coloured-hearing synaesthesia (also known as \*Chromesthesia\* or sound-to-colour synesthesia

This is where heard sounds automatically and involuntarily evoke an experience of colour.

> All six of our subjects have coloured hearing for words relating to time (throughout this paper, 'time' refers to days of the week and months of the year, but not to hours, minutes, or seconds). Some have coloured hearing for all words and many have coloured hearing for spoken letters and numbers. Furthermore, several subjects also see these percepts as vague shapes, forming spatially localised patterns in their "mind's eye".

Coloured-hearing synaesthesia seems to be different in each of the cases in Steven & Blakemore's study, including how with JF,

> When JF moves his eyes or head from left to right, his colours remain stable in space, but if he rotates his whole body, the array of colours moves with him. Hence the synaesthetic phantoms are body-centred, not oculocentric or head-centred.

I would recommend reading this study article as I found it interesting.

## How does the brain interpret a picture without a vision?

It seems that synaesthetes see colours because the visual cortex is stimulated by the sensation which triggered it. (Steven & Blakemore, 2004)

> In a single-subject fMRI study, Aleman and colleagues (2001) reported significant activation of human striate cortex when a synaesthete experienced illusory colours in response to hearing words. An earlier positron emission tomography (PET) study, however, had shown activation of visual-association cortex but not primary visual cortex in coloured-word synaesthesia (Paulesu et al 1995). Nunn et al (2002) recently supported this conclusion with their finding that cortical areas thought to be involved specifically in colour analysis (V4/V8), but not earlier visual areas, are activated when coloured-hearing synaesthetes listen to spoken words. Despite some differences in these results, it seems clear that parts of the visual cortex are activated when synaesthetes experience spurious visual sensations.

As long as there is no damage to the visual cortex, if other conditions are set for it within the brain connections, all that is needed is the correct stimulation within the visual cortex for colours to be seen.

> Sadato et al (1996), using PET, demonstrated that the visual cortex is activated when (non-synaesthetic) late-blind subjects read Braille, and others have reported activity in visual areas during non-Braille tactile discrimination in the blind (Büchel et al 1998; Burton et al 2002). Not only was primary visual cortex activated during Braille reading in the blind, but extrastriate cortex was also activated, including areas in the fusiform gyrus with Talairach coordinates corresponding to V4, which normally processes colour vision in sighted subjects (Burton 2003; Burton et al 2002). Again, this unusual visual cortical activation appears to be functionally significant, since TMS of the primary visual cortex has been shown to disrupt the ability to read Braille (Cohen et al 1997; note that TMS of V4 is not currently feasible), and it might somehow account for the fact that tactile acuity is enhanced in blindness (Goldreich and Kanics 2003)

## References

Steven M. S., & Blakemore C. (2004). Visual synaesthesia in the blind. *Perception* 33(7), 855-68
PMID: 15460512 DOI: 10.1068/p5160
**Free PDF** available from semanticscholar.org

## References in quotes from Steven & Blakemore (2004)

> Aleman A, Rutten G-J M, Sitskoorn M M, Dautzenberg G, Ramsey N F, 2001 "Activation of striate cortex in the absence of visual stimulation: an fMRI study of synesthesia" *NeuroReport* **12** 2827—2830
>
> Büchel C, Price C, Frackowiak R S, Friston K, 1998 "Different activation patterns in the visual cortex of late and congenitally blind subjects" *Brain* **121** 409—419
>
> Burton H, Snyder A Z, Conturo T E, Akbudak E, Ollinger J M, Raichle M E, 2002 "Adaptive changes in early and late blind: a fMRI study of Braille reading" *Journal of Neurophysiology* **87** 589—607
>
> Burton H, 2003 "Visual cortex activity in early and late blind people" *Journal of Neuroscience* **23** 4005—4011
>
> Cohen L G, Celnik P, Pascual-Leone A, Corwell B, Faiz L, Dambrosia J, Honda M, Sadato N, Gerloff C, Catala M D, Hallett M, 1997 \`\`Functional relevance of cross-modal plasticity in blind humans" *Nature* **389** 180—183
>
> Goldreich D, Kanics I M, 2003 "Tactile acuity is enhanced in blindness" *Journal of Neuroscience* **23** 3439—3445
>
> Nunn J A, Gregory L J, Brammer M, Williams S C R, Parslow D M, Morgan M J, Morris R G, Bullmore E T, Baron-Cohen S, Gray J A, 2002 "Functional magnetic resonance imaging of synesthesia: activation of V4/V8 by spoken words" *Nature Neuroscience* **5** 371—375
>
> Paulesu E, Harrison J, Baron-Cohen S, Watson J D, Goldstein L, Heather J, Frackowiak R S, Frith C D, 1995 "The physiology of coloured hearing: A Positron Emission Tomography activation study of coloured-word synaesthesia" *Brain* **118** 661—676
>
> Sadato N, Pascual-Leone A, Grafman J, Ibanez V, Deiber M P, Dold G, Hallett M, 1996 "Activation of primary visual cortex by Braille reading in blind subjects" *Nature* **380** 562—568
> 1 votes

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Tags: sensation
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# Question
Title: What is the meaningful difference between someone with a 145 IQ compared to a 100 IQ?
I am a lay person and new to this, and while I do understand that 145 IQ means 3 SDs up from the mean, I want to have a rough idea of what it means in real-life examples, from people who have experience in this domain. What is it that a person with a 145 IQ can typically do that a persona with a 100 IQ can typically not do? Examples of feats or the like is appreciated.

# Answer
> 13 votes
As a general note, precision in measurement of intelligence declines as you move to more extreme levels. There is greater uncertainty in measurement in the 145 range than there is at the 100 range. Norm samples get smaller, and most measures of intelligence are designed for the normal range.

**Categories:** You might find the article on IQ classification useful. The article discusses a wide range of ways to give verbal labels to IQ scores. For example, the following categories would put a 145 IQ person above "very superior" intelligence.

**Statistical interpretations:** You correctly note that 145 represents 3 standard deviations above the mean. If you assume a normal distribution and no measurement error, IQ 100 means you are more intelligent than 50% of the population, and an IQ of 145 means you are more intelligent than 99.9% of the population. Or to put another way, 1 in 2 people have an IQ greater than 100, and roughly 1 in 750 people have an IQ of greater than 145.

**Intuition:** If you went to a large representative high school (say with 500 to 1000 students), you might think of the typical student as your 100 IQ student, and the smartest kid in school as possibly being in the 145 ball park.

Another way to get some intuition is to think about the typical range IQs for various professions. As you see below, even for professions with the most intelligent people are still typically well below 145.

http://www.iqcomparisonsite.com/occupations.aspx

# Answer
> 7 votes
Consider, a *normal IQ score* falls between the range 85-115 which is approximately 70% of the population (and only 15% of people have an IQ of 115 or above), while an *extended average IQ range* tends to encompass those between 80-119 which is "x"% of the population. In order to qualify for the *International High IQ Society*, one must have an IQ of 125 or above, while entry into *Mensa* (a High IQ organization that represents the upper 2% of the population) requires an IQ of 2 standard deviations above average (or 130 and above). For the lower end of the bell curve, this will be explored later on in the post (as well as a more proper breakdown of the rest of the distribution).

*Now, what do these numbers mean?* That is, in principle, what can one do with a 100 IQ? It turns out, many studies have been done linking average IQ scores to completion of College Majors, SAT scores, and GRE (set aside the problematic elements for a moment, of which we can explore later). As for College Majors, studies have revealed a strong correlation for between those who go far into/complete specific college majors and IQ. The breakdown is as follows:

**Top End of Spectrum**

-Physics & Astronomy (133)

-Mathematical Sciences (130)

-Philosophy (129)

-Materials Engineering (129)

-Economics (128)

-Chemical Engineering (128)

-Other Engineering (128)

-Mechanical Engineering (126)

**Bottom End of Spectrum**

-Administration (107)

-Home Economics (106)

-Special (106)

-Student Counseling (105)

-Early Childhood (104)

-Social Work (103)

In order to attend College and be successful, it was found that an IQ of 110-115 is standardly required. Now, if a person with a 110-115 IQ attempted to be a Physics & Astronomy major, it has been found that they would quickly run into trouble and likely have to drop out (or fail out) early on. However, they would be successful at other college majors, some of which were listed previously. Then, an individual with a 100 base IQ has been shown to not (currently) be able to attend college successfully.

To put this in practical terms, lets take the example of those with an IQ 2 standard deviations from the norm in the adult population (2% of the population), or Physics & Astronomy combined with Mathematical Sciences Majors (closely followed by Philosophy and certain Engineering Majors, but we will limit our discussion to those past the threshold). This indicates that if we took a random sampling of 100 adults, approximately 2 would have a mind currently capable of the "brain power" necessary to do Complex Analysis or Statistical Mechanics (which is in-line with Senior level Physics or Math major cognitive abilities). As for what a 110 IQ would look like in practical terms, such a person would (currently) struggle tremendously to get a Political Science degree if they were able to attain it at all (IQ 120), while they would be able to get a degree in Business (114), Education (110), ect. See list here for more details: https://thetab.com/us/2017/04/10...

Now, IQ links to Standardized Tests such as the SAT and GRE are quite interesting as well--let us proceed with investigating the case of SAT scores. We will use the 1600 score standard (Note: a link to conversions between 2400 to 1600 score standards will be provided under Sources if one were curious). Consider, a score of 925 on the SAT (is claimed) to translate to a base 100 IQ. Here is an outline mapping out key points on the Bell Curve:

**IQ, SAT, Meaning**

* 55, 400, Trainable Moderate Mental Retardation
* 66, 525, Mild Mental Retardation
* 75, 630, Borderline Mental Retardation
* 87, 775, Dull
* 100, 935, Average
* 113, 1100, Bright
* 120, 1200, Very Bright
* 130, 1310, Extremely Bright
* 141, 1445, Briliant
* 151, 1575, Very Brilliant

For convenience, a few figures converted to the 2400 point scale (conversion chart here- https://blog.prepscholar.com/new... ):

**IQ, SAT**

* 75, 820
* 87, 1020
* 100, 1260
* 113, 1510
* 120, 1670
* 130, 1840
* 141, 2070
* 151, 2340

\[Note: There are various IQ scales, some reach to numbers higher well higher to this, this is a Standard Scales, others could be used with similar (though varying in extent) results\]

Follow this link to find an IQ Reference Table which outlines IQ ranges and typical corresponding abilities: https://www.easycalculation.com/...

Below is a transcription of the outline (IQ range, Category, Typical Ability):

1. 0-24

Profound Mental Retardation

Limited or no ability to communicate, eat, bath, dress and toilet.

2. 25-39

Severe Mental Retardation

Limited ability to communicate, eat, bath, dress and toilet. No academic skills.

3. 40-54

Moderate Mental Retardation

Some independent self-help skills and very basic academic skills.

4. 55-69

Mild Mental Retardation

Usually able to dress/bath independently and can do simple jobs. Elementary school academics.

5. 70-79

Border Line

May live independently with difficulties. Can perform simple and repetitive jobs.

6. 80-89

Low Average

Can complete vocational education and live independently.

7. 90-109

Average

Can complete high school graduation and college with difficulty.

8. 110-119

High Average

Typical level of college graduates.

9. 120-129

Superior

Typical level of persons with doctoral degrees.

10. 130-144

Gifted

Capable of understanding highly, complex academic material.

11. 145-159

Genius

intellectual ability and capable of looking beyond known facts.

12. 160-175

Extraordinary genius

Extraordinary talent like Albert Einstein

**Sources**

1. www.jstor.org.pitt.idm.oclc.org/stable/40064304?pq-origsite=summon
2. https://www.nytimes.com/roomfordebate/2011/12/04/why-should-sats-matter/the-sat-is-a-good-intelligence-test
3. http://open.lib.umn.edu/intropsyc/chapter/9-1-defining-and-measuring-intelligence/
4. open.lib.umn.edu/intropsyc/chapter/9-2-the-social-cultural-and-political-aspects-of-intelligence/
5. open.lib.umn.edu/intropsyc/chapter/9-4-chapter-summary/

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Tags: intelligence, iq
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title: Test to evaluate attention in Autism

text:
# Question
Title: Test to evaluate attention in Autism
I am looking for the most reliable and widely used tests for attention measurement in autistic persons. Can anybody help me to find such tests? I have read about some IQ tests including DAS, WASI and their sub-tests, however I didn't find any related sub-test to attention.

# Answer
> 3 votes
*You don't say what language you want the tests to be in, so I'm assuming English.*

In the book *Evidence-Based Assessment in ASD (Autism Spectrum Disorder)*, author Kenneth J. Aitken "describes and analyses a wide range of available Autism Spectrum Disorder (ASD) assessment measures". The chapter on "Attention" lists the following tests:

* Conners' Continuous Auditory Test of Attention (CATA)
* Conners' Continuous Performance Test II - Third Revision (CCPT 3)
* d2 Test of Attention (d2)
* Sustained Attention to Response Test (SART)
* Test of Everyday Attention (TEA)
* Test of Everyday Attention for Children (TEA-Ch)
* Test for Variables of Attention - 8th Edition 2015 (TOVA-8.2)

The book also explains what kind of attention each test assesses, why the test is useful in relation to Autism, and research findings.

You may want to check your local university or public library to look into a copy of that book.

---

There are many widely used, valid, and reliable tests of attention that an experienced clinician or researcher can use to assess attention in a patient with Autism. Just open any recent handbook or textbook on either attention or Autism and see what measures they use and describe.

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Tags: intelligence, autism
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# Question
Title: Why am I sometimes astonished when I doze
Why am I sometimes extremely astonished **with no reason** when I doze, especially I am really exhausted?

When I am tired and doze, I am sometimes stunned so suddenly that my whole body shakes and punches things in front, messing evrything placed in front of me. (e.g. a cup with cocoa drink, pencilcase which was open.. etc , about twice a year)

Is there any scientific reason for it?

# Answer
> 1 votes
When you are awake, the muscles in your body are always at least a little tense to keep your body in your current position. Even when you lie down (while awake) you will usually not be completely relaxed, but holding yourself "in place".

When you begin to fall asleep, your muscles relax, and depending on the position you were in, part of your body will follow gravity and begin to sink from the "tense" wakeful position into a relaxed posture. Your body notices this involuntary movement of your body parts (you may even dream of a falling sensation or some movement) and startle you awake, often with a sudden countermovement to "catch" what your subconscious perceives to be a dangerous "fall".

If you fall asleep at your desk, as you seem to do, you may well knock over something on the table in front of you, when your arms jerk forward to prevent you from falling.

It happens to all of us, except that most of us go to bed to sleep ;-)

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Tags: sleep
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# Question
Title: John Calhoun's Mouse Utopia and Genetic Diversity
I learned about John Calhoun's Mouse Utopia experiment from this Youtube video. The corresponding 1962 paper isn't readily available.

What I want to know is, did Calhoun account for genetic diversity in his experiment? Apparently he started with only a few breeding pairs, all white lab mice.

# Answer
## Quick (short answer)

No, Calhoon did not account for genetic diversity in his experiments outlined in your question.

## Full answer

Reading the article you mentioned, Calhoun (1962) started with wild Norway Rats, also referred to as common rats, brown rats, street rats, sewer rats, or Hanover rats.

> I confined a population of wild Norway rats in a quarter-acre enclosure. 'With an abundance of food and places to live and with predation and disease eliminated or minimized, only the animals' behavior with respect to one another remained as a factor that might affect the increase in their number. There could be no escape from the behavioral consequences of rising population density. By the end of 27 months the population had become stabilized at 150 adults. Yet adult mortality was so low that 5,000 adults might have been expected from the observed reproductive rate. The reason this larger population did not materialize was that infant mortality was extremely high. Even with only 150 adults in the enclosure, stress from social interaction led to such disruption of maternal behavior that few young survived.

Then he turned to a domesticated albino strain of the Norway rat under more controlled circumstances indoors, and

> The data for the present discussion come from the histories of six different populations. Each was permitted to increase to approximately twice the number that my experience had indicated could occupy the available space with only moderate stress from social interaction. In each case my associates and I maintained close surveillance of the colonies for 16 months in order to obtain detailed records of the modifications of behavior induced by population density.

There is very little genetic variation in brown rats (Ness, et al. 2012), no matter where in the world you collect them (Ness, 2013). Therefore, apart from the fact that the article was discussing data on a **domesticated albino strain** of the Norway rat, all the experiments mentioned used brown rats. There were no black rats, mole rats, or any other kinds of rat used.

## References

Calhoun, J.B. (1962). Population density and social pathology. *Scientific American*, 206, 139—48.

Ness, R. W., Zhang, Y.-H., Cong, L., Wang, Y., Zhang, J.-X., & Keightley, P. D. (2012). Nuclear Gene Variation in Wild Brown Rats. G3: Genes|Genomes|Genetics, 2(12), 1661—1664.
DOI: 10.1534/g3.112.004713 PMCID: PMC3516487

Ness, R. (2013). Genetic diversity of wild brown rats \[Online\]
Retrieved from: http://sites.utm.utoronto.ca/ness/blog/01182016-1515/genetic-diversity-wild-brown-rats
> 5 votes

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Tags: social-psychology, methodology, experimental-psychology, animal-cognition
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# Question
Title: Intuition behind loss quadrant of prospect theory
This picture summarizes prospect theory by Daniel Kahneman.

Looking at the gains part: The slope of the graph is getting smaller. I can understand this: If I own a million, then adding 100 euro's isn't as impactful as when I own only 1 euro.

My question is about the losses part: Here also the slope of the graph is getting smaller away from the reference point. This implies that if someone would either lose 100 euro or have a 50% chance of losing 200 euro, he would go for the gamble and become risk seeking.

But to me this doesn't make intuitive sense for two reasons:

1. If I am loss-averse, which I am, then why would I take a gamble with my second 100 euro's? I would look at it as if I already lost 100 euros and then I can take the gamble of 50% of winning 100 euro or 50% losing another 100 euro. Since I am loss-averse I would not take the bet.
2. Let's say I only own 200 euro in total: in that case I would definately want to hold on to my last 100 euro, since then I can at least pay for the rent. In other words, the utility of my last 100 euro is way bigger than the utility of my second-last 100 euro. But this is not represented in the slope.

Can anyone explain to me why according to Kahneman the slope of the losses-part diminishes away from the reference point?

# Answer
> 1 votes
Prospect theory states that people make decisions based on the potential value of losses and gains rather than the final outcome, and that people evaluate these losses and gains using certain heuristics (risk potentials) - Source.

When you look at Prospect theory graphs, you need to remember that it is all about **perceived potentials**. (Perceived potential gains/losses against the perceived potential value).

Let's look at the logic to start with. If the potential value of the prospective task is negative, **it is perceived** that the outcome result has a higher potential to be negative (loss); and the opposite is true also. If the potential value of the prospective task is positive, **it is perceived** the outcome result has a higher potential to be positive (win or gain).

Now with the logic in place, more potential loss perceived will result in a perceived potential of a more negative outcome and more potential gain perceived will result in a perceived potential of higher gains.

The line crosses the $0,0$ $x,y$ axes because it is perceieved that a zero potential value will result in zero loss or gain and the potential losses increase as you move nagatively away from the $0,0$ reference point, and the losses diminish as you move positively away from the $0,0$ reference point.

Now you also have to factor the probability of win or lose into the equation. With low expactation of any gains (low perceived value) it doesn't matter if you win or lose, it is perceived that you are going to lose overall. With high expectation of gains, (high perceived value), you need to have a win in order to achieve the gain perceived.

If you also rotate the graph, you get this

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Tags: cognitive-psychology, decision-making
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# Question
Title: What's the difference between Confirmation Bias and the Affect Heuristic?
I've been reading "Thinking Fast & Slow," by Daniel Kahneman. At the end of Chapter 9, he introduces the "Affect Heuristic," a concept introduced by Paul Slovic that effectively states that people let their likes and dislikes determine their beliefs about the world.

Isn't this just an extension of confirmation bias - e.g. that people look for confirming evidence when evaluating ideas? It seems obvious that if you like something or dislike a concept, you'll search for evidence to affirm your preexisting position. For example - if I was a conservative and I learned of a bill introduced by a liberal politician, I'd naturally make the assumption that the bill is misguided and search for evidence to confirm that assumption (and vice-versa).

What's the difference between them? I'm having trouble defining the "Affect Heuristic" clearly in my mind.

# Answer
Confirmation bias is the tendency to search for, interpret, favour, and recall information in a way that confirms pre-existing beliefs or hypotheses (WikiPedia; Plous, 1993)

The affect heuristic is a mental shortcut that allows people to make decisions, and solve problems quickly and efficiently, in which current emotion - fear, pleasure, surprise, etc. - influences decisions.

> In other words, it is a type of heuristic in which emotional response, or "affect" in psychological terms, plays a lead role. (WikiPedia)

Or in the words of Slovic,

> As used here, ‘‘affect’’ means the specific quality of ‘‘goodness’’ or ‘‘badness’’ (Slovic, et al. 2007)

They can sound similar, and in a way they can be; but generally they are different. With confirmation bias, I would be looking for something to back up a belief I *“know”* is correct, while I may or may not like this belief,

> it is the only correct answer!

This is different to the affect heuristic, where I don’t like the proposition put forward by others and so I am going to look for evidence to back the ideas I like.

## --Edit for further clarification after comment--

You could say

> You can search for evidence to confirm something is right if you believe it's right, and you can search for evidence to confirm something is wrong if you believe it's wrong

and that is true. That would be Confirmation Bias if you are searching purely for evidence to prove your **belief based on what is known**. Let's look at the difference in another way.

### Scenario where there are two opposing points of view ($X$ and $Y$).

$X$ has a conclusion based on plenty of evidence which is corroborated by many unbiased studies.
$Y$ has a conclusion which is also based on plenty of studies which corroborates each other.
**However**, there were flaws in some studies and others were biased due to undeclared financial interests with some participants.

**When there is no bias**, you are completely open minded and you would be taking an unbiased viewpoint on the evidence presented, therefore it would be fair to assume that $X$ is true and $Y$ is false. When looking for more evidence, you are looking for evidence for and against both $X$ and $Y$.

**When there is *Pure* Confirmation Bias, you totally accept** $X$ being true, and it fits with your beliefs and way of life, and when looking for more evidence, you are looking to strengthen that truth with more evidence to back $X$ and more evidence to refute $Y$.

**When there is Confirmation Bias with Affect Heuristics**, this can be where you don't like viewpoint $X$ because it doesn't fit with your beliefs. You can accept $X$ being true, but there is the counteracting wish for $Y$ to be true.

There can be affect heuristics involved when looking for any strong counteracting evidence, yet you are still accepting that $X$ is true, so whilst looking for counteracting evidence, you are also looking for evidence confirming $X$. You could be forgiven for thinking that this is unbiased research, but it is not unbiased, because you wish for $Y$ to be true as you have a vested interest in $Y$ but you also accept $X$.

**When there are *pure* Affect Heuristics, you cannot accept** $X$ as true because of your beliefs, or because it adversely affects your way of life, and when looking for more evidence, you are looking for evidence to back $Y$ and plenty of evidence to refute $X$.

**References**

Plous, S. (1993). *The Psychology of Judgment and Decision Making.* New York: McGraw-Hill p.233

Slovic, P., Finucane, M. L., Peters, E., MacGregor, D. G. (2007). The affect heuristic. *European Journal of Operational Research* 177(3),1333–1352
DOI: 10.1016/j.ejor.2005.04.006
> 0 votes

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Tags: cognitive-psychology, bias, behavioral-economics
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# Question
Title: Are there any negative effects from hypnotherapy for bipolar disorder?
My wife has been diagnosed with Bipolar disorder and as her husband and care giver I'm trying to delve into both understanding this disease and being an intelligent guide to freedom from as many of the negative symptoms as is possible. I've been reading up on hypnotism and would like to consider it as a future treatment but I'm wondering if the nature of Bipolar creates any unique environments where hypnotism might harm rather than heal.

# Answer
> 2 votes
## Preamble

First of all, I would like to point out that hypnosis, and therefore hypnotherapy, is generally considered pseudo-scientific within the scientific community and therefore this question can be classed as off-topic here by some. However, there are trained and licensed hypnotherapists who share the same question on whether or not to use hypnotherapy on patients diagnosed with Bipolar Disorder (Leach, 2013), so I will provide some background to my answer with some research available.

## Is hypnotherapy suitable for Bipolar Disorder?

Switches into mania have been observed in unipolar and bipolar depressed patients following physical treatments as well as cognitive therapy. Such a phenomenon has not been observed with hypnotherapy (Suresh & Srinivasan, 1994 - Introduction)

Suresh & Srinivasan studied the possibility of hypnotherapy being used to help Bipolar Disorder with a patient suffering from Dysthymic Disorder (now called Persistent Depressive Disorder) which is less acute and severe than major depressive disorder.

> Three sessions of hypnotherapy were given over a period of one week. Ventilation of her negative self evaluations and use of positive suggestions to improve her self esteem and ego strength was done during each session under first stage of hypnosis. Neither deep level of hypnosis nor hypnoanalysis was attempted. After the initial sessions, the patient was instructed to practice self-hypnosis once a day using an audio cassette with a recording of the last session by the therapist.

A point to note with this study is that **hypnotherapy was advised for the patient as she did not prefer drug therapy** and there were major problems.

> At the end of one week she presented with a cheerful mood and improved self-esteem, confidence and energy with no depressive symptoms. Her child was concurrently treated and had by then returned to school. Self-hypnosis was continued and ten days later her spouse brought her with symptoms of sleeplessness, irritability with a tendency to be aggressive and disinhibited, excessive talk, ideomotor pressure and grandiose ideation. Clinical examination showed the presence of a Manic disorder.
>
> Following recovery from this episode in two weeks with antipsychotics, she was advised not to practice self-hypnosis. However, this was not heeded and a week later there was reemergence of manic symptoms requiring increase in the dose of antipsychotics. Subsequently, it was ensured that she did not practice self-hypnosis.

Suresh & Srinivasan noted that as deep hypnosis or hypnoanalysis was carefully avoided, the manic reaction could not be viewed as a manifestation of nonspecific psychotic disorganisation which is known to occur if hypnotherapy is too deep and uncontrolled (Auerbach, 1962); and the precipitation of mania by hypnotherapy supports the evidence that this therapy can be useful in depression.

Although Psychotherapy using hypnosis is known to be helpful in mild depression if **light hypnosis and simple positive suggestions** are applied (Ambrose & Newbold, 1980), I would contest this last statement by Suresh & Srinivasan, by pointing out that antipsychotics were prescribed at the time of mania being present, and therefore you cannot say that it was the hypnotherapy which precipitated mania.

## The bottom line - Talk to your doctor

As a trained and accredited hypnotherapist myself, the bottom line is that hypnotherapists are told in accredited training that they **must not** provide hypnotherapy to those diagnosed with a psychosis or certain types of personality disorder, as it could make your condition worse. (**See also, neurosis vs psychosis**) Another golden rule is that anyone who is looking to embark on hypnotherapy when they are diagnosed with any mental health condition should obtain doctor's permission first.

## References

Ambrose, G. & Newbold, G.(1980). *A Handbook of Medical Hypnosis, 4th edition*. London: Bailliere Tindall.

Auerbach, A. (1962). Attitudes of Psychiatrist to the use of hypnosis. *Journal of American Medical Association*, 180(11), 917—921.
DOI: 10.1001/jama.1962.03050240013003

Leach, H. (2013). *My experience of mental health discrimination as a hypnotherapist* \[Online\]
Available at: https://www.time-to-change.org.uk/blog/hypnotherapist-mental-health-discrimination

Suresh, T. R., & Srinivasan, T. N. (1994). Mania following hypnotherapy. *Indian Journal of Psychiatry*, 36(1), 34—35.
PMCID: PMC2972454 \[Free PDF\]

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Tags: bipolar-disorder, hypnosis
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# Question
Title: Does the lexical hypothesis have any role in 'creativity'?
The lexical hypothesis was used to I think *create* the 5 factor model of personality.

Has anything similar been done in the science of 'creativity'?

While, clearly, "creativity" is a component of intelligence, even if it is also one in personality.

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What got me thinking about this, is the measurement of 'creativity', which is I think notoriously difficult, even more so that aptitude in general. Specifically, I was thinking about how it seems that 'fluency' seems lexically close to some terms close to creativity.

How would *general* cognitive fluency, as it is measured by cognitive test, correlate with creativity?

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fluency, noun

* the ability to express oneself easily and articulately.

fantasy, noun

* a fanciful mental image, typically one on which a person often dwells and which reflects their conscious or unconscious wishes

imagination, noun

* the faculty or action of forming new ideas, or images or concepts of external objects not present to the senses.

etc.

# Answer
> 1 votes
Jauk et al. (2013) talks about the relationship between intelligence and creativity whilst King, et al. (1996) talks about the the relationship between the 5-factor model and creativity.

> **4.2. Personality predictors of creative potential**
>
> When performing separate multiple regression analyses in samples of lower and higher intelligence, we found that openness to experiences predicts creative potential in the subsample above the threshold whereas conscientiousness is negatively related to creative potential in the lower IQ range.
>
> While it is well documented that that there exists a positive association between openness and creative potential (Batey & Furnham, 2006; Feist, 2010; King et al., 1996), the present result points to an interaction between intelligence and openness: High creative potential is not possible with a low level IQ; but once the intelligence threshold is met, openness may explain to some extent whether the required cognitive disposition is actually turned into high creative potential (Jauk, et al. 2013)

**References**

Batey M., Furnham A. (2006). Creativity, intelligence, and personality: A critical review of the scattered literature. *Genetic, Social, and General Psychology Monographs*. 132(4) 355–429.
PMID: 18341234

Feist G.J. (2010). The function of personality in creativity: The nature and nurture of the creative personality. In: Kaufman J.C., Sternberg R.J., editors. *The Cambridge handbook of creativity*. New York: Cambridge University Press; pp. 113–130.

Jauk, E., Benedek, M., Dunst, B., & Neubauer, A. C. (2013). The relationship between intelligence and creativity: New support for the threshold hypothesis by means of empirical breakpoint detection. *Intelligence*, 41(4), 212–221.
DOI: 10.1016/j.intell.2013.03.003

King L. A., Walker L. M. & Broyles S. J. (1996). Creativity and the five-factor model. *Journal of Research in Personality*. 30(2), 189–203.
DOI: 10.1006/jrpe.1996.0013

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Tags: personality, creativity
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title: Computer-based cognitive tests

text:
# Question
Title: Computer-based cognitive tests
Maybe someone can point me out on the computer-based set of tests to assess the cognitive abilities of the adults? I am looking for something like ETS cognitive tests KIT that can be used online for the research purposes.

# Answer
> 2 votes
A quick Google search reveals a list of computer-based cognitive testing software. Apparently,

* Cogstate computerized cognitive tests

> have been used in hundreds of clinical trials––guiding decision-making for safety and efficacy across many indications and all phases of development.
* CANTAB Connect Research

> is the world’s most validated, precise and reliable research software providing sensitive digital measures of cognitive function for all areas of brain research. Delivering leading neuroscience through our secure cloud platform, CANTAB Connect Research is an efficient and easy-to-use system providing insights into behaviours, underlying brain circuits and neurochemical systems and measurement of digital cognitive biomarkers.

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Tags: measurement, test, study-cognitive-sciences
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# Question
Title: What is the difference between Avolition and Laziness?
What is the difference between Laziness and Avolition?

They seem behaviorally similar. Is the difference cognitive perhaps?

# Answer
> 9 votes
Robin Kramer gave a good starting point in his comment.

As he said, the difference between laziness and avolition primarily come from the causes of each behavior. Laziness is common among psychologically "normal" individuals while avolition is commonly seen in patients with schizophrenia or depression. Now I will go in depth with each to better characterize them and hopefully show the differences between the two. I will talk about avolition first because it is better defined in the field of psychology.

**Avolition**

Definition of avolition mainly comes from research of schizophrenia symptoms. Schizophrenia symptoms can be divided as positive and negative symptoms. Negative symptoms can be divided into diminished expression and amotivation. Amotivation consists of anhedonia and avolition (Foussias & Remington, 2008). Anhedonia is diminished capacity to experience pleasant emotions. Avolition is the loss of drive and lack of curiosity. Avolition occurs in depression as well but is different for the two disorders. Avolition comes with saddening or depressed effect for people with depression, but this is not the case for people with schizophrenia.

Since activation of prefrontal cortex is generally associated with initiation of spontaneous activity (which is less in frequency in people with avolition), hypoactivation of prefrontal cortex may be the cause of avolition in patients with schizophrenia (Sebanz & Prinz, 2006). Another study shows anti-correlation between dorsal caudate activity and negative symptoms of schizophrenia including avolition (Mucci et al., 2015). This indicates that avolition may be caused by abnormalities in the motivation-related circuit. There are two networks known to be involved in motivation-related brain network: first one includes the ventral striatum, orbito-frontal cortex (OFC), insula, and medial prefrontal cortex (mPFC) and is involved in liking, reward anticipation, reward valuation, and representation of stimulus-reward associations. The other circuit includes the dorsal caudate and the dorsolateral prefrontal cortex (DLPFC), and is involved in representation of the expected reward and causal connection between action and reward (Liljeholm et al., 2011). Thus, there is a theory that patients with schizophrenia may exhibit avolition because they are not able to anticipate reward from their actions.

**Laziness**

Laziness itself is not studied extensively in psychology primarily because it has not been well-defined. At first glance, laziness seems to be a familiar concept to the usual people. However, laziness may involve many factors of human behavior that are at times but not always exhibited in people considered to be lazy. For example, one of the requirements of being lazy may be having no motivation. Without motivation, the person is less likely to show desire to take certain actions. But plenty show desire and motivation; these motivations are just not targetted to a long term goal. With these difficulties in mind, I personally believe that one of the economics definitions of laziness is most in line with what people commonly refer to as laziness: tendency for people to focus on the activities that give immediate pleasure rather than longer-term activities (Frédéric Bastiat, 1850). Bastiat called it idleness rather than laziness, but I believe they are synonymous in this context.

For the cause of laziness, I must confess this is not something I am familiar with. However, popular sources such as this one state that there can be multiple causes for laziness. One would be lack of interest in the field itself. Another would be lacking faith that the action will be worth the effort - which is similar concept to learned helplessness. One study states that anterior frontomedian cortex is involved in making these internal judgements leading to decision making (Zysset et al., 2002). However, studies such as this does not show what causes change in the activation of the anterior frontomedian cortex.

I also noticed that a popular YouTube video about laziness refers to a mouse study that selectively bred physically active mice which led to physically active mice descendents having the same characteristics. The video uses this study to state that there are genetic factors involved in laziness. Not only is it a stretch to make a connection between laziness of humans and tendency to wheel run by mice, the study itself is flawed in that the mice were bred with their parents for the first few weeks. This means that environmental factors cannot be ruled out. Here's the paper if you want to take a look.

**References**

Bastiat, Frédéric. Economic Harmonies. George B. de Huszar, trans. and W. Hayden Boyers, ed. 1996. Library of Economics and Liberty. Retrieved May 29, 2016 from the World Wide Web: http://www.econlib.org/library/Bastiat/basHar20.html

Foussias, G., & Remington, G. (2010). Negative Symptoms in Schizophrenia: Avolition and Occam’s Razor. Schizophrenia Bulletin, 36(2), 359–369. http://doi.org/10.1093/schbul/sbn094

Leon F Seltzer (2008). Laziness: Fact or Fiction?. https://www.psychologytoday.com/blog/evolution-the-self/200806/laziness-fact-or-fiction

Liljeholm, M., Tricomi, E., O’Doherty, J. P., & Balleine, B. W. (2011). Neural correlates of instrumental contingency learning: Differential effects of action-reward conjunction and disjunction. The Journal of Neuroscience, 31(7), 2474–2480. http://doi.org/10.1523/JNEUROSCI.3354-10.2011

Mucci, A., Dima, D., Soricelli, A., Volpe, U., Bucci, P., Frangou, S., … Maj, M. (2015). Is avolition in schizophrenia associated with a deficit of dorsal caudate activity? A functional magnetic resonance imaging study during reward anticipation and feedback. Psychological Medicine, 45(8), 1765–1778. http://doi.org/10.1017/S0033291714002943

Sebanz, Natalie (Ed); Prinz, Wolfgang (Ed) Cambridge, MA, US: MIT Press Disorders of volition. (2006). vii 493 pp.

Stefan Zysset, Oswald Huber, Evelyn Ferstl, D.Yves von Cramon, The Anterior Frontomedian Cortex and Evaluative Judgment: An fMRI Study, NeuroImage, Volume 15, Issue 4, April 2002, Pages 983-991, ISSN 1053-8119, http://dx.doi.org/10.1006/nimg.2001.1008. (http://www.sciencedirect.com/science/article/pii/S1053811901910080)

# Answer
> 2 votes
Supposing that by "laziness" you just mean behaviours etc. apparently identical to avolition, then the difference is, assuming we call "avolition" a symptom of an *illness*, that **avolition is *out of the control of the sufferer***, unlike laziness.

That's if we do agree that illness is out of a sufferers control, at least more so than their other behaviours. That is Fulford's 1989 attractive definition of illness:

> failures of action that are beyond the abilities of a person

Naturalism in the Philosophy of Health, p72

Whether or not we call that "cognitive", as you ask in the question, may be less interesting than asking how we *know* that something is out of our control (presumably via introspection), and how it can be (presumably just biological if the mind is the brain).

**References**

Fulford, K. W. M. (1989). Moral theory and medical practice. Cambridge University Press.

Giroux, E. (2016). *Naturalism in the Philosophy of Health: Issues and Implications*. Switzerland: Springer International Publishing
DOI: 10.1007/978-3-319-29091-1

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Tags: terminology, willpower
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# Question
Title: How can I test whether Dorsal Raphe Nucleus (DRN) activity at night is related to variations in mood?
I'm reading this paper, which discusses Serotonin activity in the Dorsal Ralphe Nucleus(DRN), and even includes some mathematical models of how serotonin is released and reabsorbed. The paper states that depressed patients show significant decreases in serotonin both in DRN and outside. The thing that impressed me about this paper is that it gives examples of the **serotonin concentration in DRN in normal person, compared to depressed patient, and the difference is about 80%**

Bursts and the Efficacy of Selective Serotonin Reuptake Inhibitors

The paper above referenced this excellent paper on how DRN is involved in the regulation of motor activity, and even includes some references to how **DRN is involved in the sleep/wake cycle**.

5-HT and motor control: a hypothesis

Here's an example of a graph from the article above. It shows how the firing rate of the DRN increases in response to cat's grooming, compared to quiet wakefulness. DRN firing pattern changes in response to movement. Can I reverse this statement to say that **movement indicates DRN activity?**

**The hypothesis that I have is that if less Serotonin is available in the DRN as a result of depression, the activity of the DRN as related to motion at night would be different from the normal person.** I hypothesize that by observing the motion of human in bed at night, it may be possible to quantify the activity of DRN, potentially using this information to predict mood fluctuations.

Here's my train of thought - DRN fires differently in response to motion, and motion is accompanied by DRN firing, while muscle atonia is accompanied by total lack of firing. An actigraph has shown that a person (myself and others) moves over the course of the night, in bursts with episodes of total stillness and episodes of burst activity. People move differently in different sleep stages. In cats without atonia (see figure below), DRN gets activated when Rapid Eye Movement(REM) sleep is detected, in response to the cat's actions within the dream, similar to the waking state.. Normally, DRN shows absolutely no firing pattern during REM sleep. **I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days**, where depression can be linked to decreased levels of Serotonin in DRN cells.

If I understand the Bursts and the Efficacy of Selective Serotonin Reuptake Inhibitors paper correctly, bursts of electrical activity within the DRN alter Serotonin concentrations for some time after the burst. As such, it seems to me that bursts of electrical activity associated with motion (a typical motion at night is 3-10 seconds) with a large motion observed every 2-3 minutes over the 20 or so minute period that preceedes awakening would have an impact on the Serotonin concentration in the DRN.

I'm trying to understand if activation of Dorsal Raphe Nucleus during Rapid Eye Movement sleep can be detected with an **iPhone actigraph**, and if this activation can be quantified, measured and correlated to behavior in the preceeding and subsequent few days. I'm looking to correlate activation of DRN or lack of thereof with the normal, elevated or depressed moods and activity patterns.

An iPhone actigraph measures gross motor activity, which I guess would roughly compare to the EMG from the images above. In this case, the plot is logarithmic, with taller redder bars being orders of magnitude bigger than the baseline "noise" observed by the device.

Over the past year I've been working on an iPhone actigraph - an app that analyzes user's motion and can be used for sleep studies. On that actigraph, I'm seeing spikes in motion (my sleep) at different sleep phases. The device allows marking of events over night - midnight awakenings, and dream awakenings.

Here's an example of a sleep cycle graph that is drawn based on the observed motion at night. In this case, the deeper the graph, the more still the person is. Red circles indicate insomnia, green circles indicate subsequent dream awakenings.

The device also allows the user to track moods over the course of the day with a very cool Pick A Mood scale and add different events, such as meals, exercise and over 80 other types of events.

Since I'm only an amateur at science and sleep studies, **what are your thoughts on the train of thought above? Is there any merit to the hypothesis?** How would I go about testing it with the technology I outlined?

Thank you for your input!

# Answer
**Short answer**
To start my post with a cliche - correlation (between raphe activity and movement) does not imply causality. More importantly, the complete absence of the raphe nucleus does not negate movement.

**Background**
Although I cannot disprove your hypotheses, I do wish to express a word of caution (6 years after your post :-)

> Can I reverse this statement to say that movement indicates DRN activity?

I would be careful with this statement. Activity in the raphe nucleus is positively correlated with behavioral arousal, yes (Ranade & Mainen, 2009). Further, raphe activity is thought to be related to the level of tonic motor activity associated with gross motor activity and repetitive, central pattern generator mediated responses (Jacobs & Fomal, 1997). Yet, to couple these findings in reverse, and state that one can measure raphe activity through movement detection is tricky. Importantly, there are hosts of studies **where the raphe nucleus was ablated and animals still showed (quite normal) motor activity** (*e.g.* Ghaderi *et al*. (2012)).

> I would like to examine the pattern of movement over night and compare it to the feeling of well being in subsequent days.

It has been shown that successful treatment of depression results in an increase of motor activity. As depression is strongly linked to serotonin signaling this may be an interesting side track. However, increased motor activity was only found for day-time level of movements; clinical improvement was not reflected by night-time measurements. In case of depression, it is thought that activity in the frontal lobe is associated with motor impairments in depression and is related more top dopamine transmission than
serotonin (Todder *et al*., 2009). Indeed, the motor system is regulated more directly through dopaminergic neurons (think Parkinson).

> what are your thoughts on the train of thought above? Is there any merit to the hypothesis?

I think there is merit, but using movement detection with an iphone app, and thinking that a correlation between movement and serotonin signalling implies a causal relation between raphe activity and movement is dodgy. You have to prove this first, either by a solid literature search or through experimental investigation and find support for your hypothesis.

<sub>**References**
**-** Ghaderi *et al*. *Procedia - Social Behav Sci* (2012); **32**: 403-10
**-** Jacobs & Fomal, *Curr Opinion Neurobiol* (1997); 7(6): 820-5
**-** Ranade & Mainen, *J Physiol* (2009); **102**(5): 3026-37
**-** Todder *et al*., *World J Biol Psych* (2009); **10**(4): 276-84</sub>
> 2 votes

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Tags: neuroscience, theoretical-neuroscience, mood
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# Question
Title: How does one escape learned helplessness?
I've been researching learned helplessness lately, an idea that seems to be responsible for much of the negative behavior observed in humans. Basically, the idea is that once repeatedly exposed to an inescapable pain, a subject learns to accept the pain even when it becomes avoidable.

This was first described by Martin Seligman who observed such behavior in dogs, who, upon being placed in a box that would shock them at random times and then moved to a box where the shock could be escaped by jumping over a barrier, refuse to even attempt to jump the barrier to escape, whereas dogs that could stop the shock in the first box with a lever would easily jump the barrier.

In all my research, however, it seems that the "learned helplessness" could only be unlearned by manually moving the dogs' legs to simulate the behavior to overcome the obstacle. However, in humans, such helplessness situations are often very abstract, for example the idea that no matter how hard one works they will never be able to escape debt, or pay their taxes. In such cases, "manually moving people's legs" is anywhere from extremely impractical to impossible. Does this mean that human learned helplessness is most cases is insurmountable?

How in the case of abstract helplessness conditions can human learned helplessness be escaped?

# Answer
> 5 votes
## History

Martin E. P. Seligman, has written extensively on the nature, etiology, and significance of learned helplessness, and in 1975, he broadened the scope of learned helplessness from animal behaviour to a wide variety of human behaviours, including reactive depression, stomach ulcers, voodoo deaths, and child development, then in 1978, he criticised and reformulated his hypothesis.

> The old hypothesis, when applied to learned helplessness in humans, has two major problems: (a) It does not distinguish between cases in which outcomes are uncontrollable for all people and cases in which they are uncontrollable only for some people (universal vs. personal helplessness), and (b) it does not explain when helplessness is general and when specific, or when chronic and when acute. A reformulation based on a revision of attribution theory is proposed to resolve these inadequacies. (Seligman, 1978)

Seligman then went on to rectify these deficiencies.

## Problem (a): universal vs. personal helplessness

### Universal Helplessness

> Suppose a child contracts leukemia and the father bends all his resources to save the child's life. Nothing he does, however, improves the child's health. Eventually he comes to believe there is nothing he can do. Nor is there anything anyone else can do since leukemia is incurable. He subsequently gives up trying to save the child's life and exhibits signs of behavioral helplessness as well as depressed affect. This example fits the specifications of the old learned helplessness hypothesis. The parent believed the course of the child's disease was independent of all of his responses as well as the responses of other people. We term this situation *universal helplessness* (Seligman, 1978).

In the same paper, Seligman considered universal helplessness to be **externally attributed**. Situations where people believe that neither they nor relevant others can solve the problem are instances of universal helplessness according to the 1978 hypothesis.

### Personal helplessness

> Suppose a person tries very hard in school. He studies endlessly, takes remedial courses, hires tutors. But he fails anyway. The person comes to believe he is stupid and gives up trying to pass. This is not a clear case of uncontrollability according to the old model, since the person believed there existed responses that would contingently produce passing grades although he did not possess them. Regardless of any voluntary response the person made, however, the probability of his obtaining good grades was not altered. We term this situation *personal helplessness* (Seligman, 1978).

In the same paper, Seligman considered personal helplessness to be **internally attributed**. Situations in which people believe they cannot solve solvable problems are instances of personal helplessness according to the 1978 hypothesis.

### Flow of events leading to helplessness

The 5 steps towards helplessness was outlined in Seligman's 1978 paper (Page 52 - bold emphasis mine).

1. ***Objective*** non-contingency
2. ***Perception*** of present **and** past non-contingency
3. ***Attribution*** for **present or past** non-contingency
4. ***Expectation*** of **future** non-contingency
5. *Symptoms* of helplessness

> Objective noncontingency is predicted to lead to symptoms of helplessness only if the expectation of noncontingency is present (Seligman, 1975 & 1978).

Pre-1978, Seligman's model was vague in specifying how perception that events are non-contingent (past or present) was transformed into an expectation that events will be non-contingent in the future.

> Our reformulation regards the attribution the individual makes for noncontingency between his acts and outcomes in the here and now as a determinant of his subsequent expectations for future noncontingency. These expectations, in turn, determine the generality, chronicity, and type of his helplessness symptoms. In the context of this general account of the role of attribution in the production of symptoms, the distinction between universal and personal helplessness can now be clarified.
>
> ...
>
> Cognitive and motivational deficits occur in both personal and universal helplessness. Abramson (1977) has demonstrated this empirically while showing that lowered self-esteem occurs only in personal helplessness (Seligman, 1978).

## Problem (b): general vs. specific helplessness, and chronic vs. acute helplessness

When helplessness deficits occur in a broad range of situations, they are called them *global* or *general helplessness*; when the deficits occur in a narrow range of situations, they are called *specific helplessness*.

Some helplessness deficits may last only minutes and others may last years. Helplessness is considered to be *chronic* when it is either long-lived or recurrent and *transient* or *acute* when short-lived and non-recurrent (Seligman, 1978).

## Your Question - How can human learned helplessness be escaped?

Seligman, in his 1978 paper touched on this in a number of ways.

> The subject is presented with an unsolvable problem, tested on a second solvable task, and finally debriefed. The subject is told that the first problem was actually unsolvable and therefore no one could have solved it. Experimenters in human helplessness studies seem to believe that telling a subject that no one could solve the problem will cause helplessness deficits to go away. The prior discussion suggests that convincing a subject that his helplessness is universal rather than personal will remove self-esteem deficits suffered in the experiment (Seligman, 1978).

He also outlined some general observations.

* Those who typically attribute their failures to general, stable, and internal factors will be more prone to general and chronic helplessness depressions with low self-esteem.
* Beck (1967) argued similarly that the pre-morbid depressive is an individual who makes logical errors in interpreting reality. For example, the depression-prone individual overgeneralises; a student regards his poor performance in a single class on one particular day as final proof of his stupidity.
* Boys and girls have been found to differ in attribution styles, with girls attributing helplessness to lack of ability (global, stable) and boys to lack of effort (specific, unstable) (Dweck, 1976).

> Therefore, the therapeutic implications of the reformulated hypothesis can now be schematized.

Seligman went on to state that depression is most far reaching when

1. **the estimated probability of a positive outcome is low or the estimated probability of an aversive outcome is high,**
> Change the estimated probability of the outcome. Change the environment by reducing the likelihood of aversive outcomes and increasing the likelihood of desired outcomes.
2. **the outcome is highly positive or aversive,**
> Make the highly preferred outcomes less preferred by reducing the aversiveness of unrelievable outcomes or the desirability of unobtainable outcomes.
3. **the outcome is expected to be uncontrollable,**
> Change the expectation from uncontrollability to controllability when the outcomes are attainable. When the responses are not yet in the individual's repertoire but can be, train the appropriate skills. When the responses are already in the individual's repertoire but cannot be made because of distorted expectation of response-outcome independence, modify the distorted expectation. When the outcomes are unattainable, this does not apply.
4. **the attribution for this uncontrollability is to a general, stable, internal factor.**
> Change unrealistic attributions for failure toward external, unstable, specific factors, and change unrealistic attributions for success toward internal, stable, global factors. The model predicts that depression will be most far-reaching and produce the most symptoms when a failure is attributed to stable, global, and internal factors, since the patient now expects that many future outcomes will be noncontingently related to his responses. Getting the patient to make an external, unstable, and specific attribution for failure should reduce the depression in cases in which the original attribution is unrealistic. The logic, of course, is that an external attribution for failure raises self-esteem, an unstable one cuts the deficits short, and a specific one makes the deficits less general

In 1983, learned helplessness was also proposed as a model for the emotional numbing and maladaptive passivity sometimes following victimisation. Victims may learn during the victimisation episode that responding is futile

> If this learning is represented as a general expectation of helplessness, then subsequent deficits may occur in situations unrelated to the original situation in which the victimization occurred. The victim’s causal interpretation of the victimization episode may partly determine the chronicity and generality of these deficits, and the involvement of self-esteem. (Peterson & Seligman, 1983).

Based on Seligman's findings, Cognitive Therapy might be beneficial as:

> Therapy may consist of testing the assumptions which one makes and looking for new information that could help shift the assumptions in a way that leads to different emotional or behavioral reactions. Change may begin by targeting thoughts (to change emotion and behavior), behavior (to change feelings and thoughts), or the individual's goals (by identifying thoughts, feelings or behavior that conflict with the goals).

## References

Abramson, L. (1977). Universal versus personal helplessness: An experimental test of the reformulated theory of learned helplessness and depression. ***Unpublished doctoral dissertation, University of Pennsylvania***.

Beck, A. T. (1967) *Depression: Clinical, experimental and theoretical aspects*. New York: Hoeber.

Dweck, C. (1976). Children's interpretation of evaluative feedback: The effect of social cues on learned helplessness. *Merrill-Palmer Quarterly of Behavior and Development*, 22(2), 105-109.
Retrieved from http://www.jstor.org/stable/23083956

Peterson, C., & Seligman, M. E. (1983). Learned helplessness and victimization. *Journal of Social Issues*, 39(2), 103—116.
DOI: 10.1111/j.1540-4560.1983.tb00143.x

Seligman, M. E. P., & Maier, S. F. (1967). Failure to escape traumatic shock. *Journal of Experimental Psychology*, 74(1), 1—9.
DOI: 10.1037/h0024514

Seligman, M. E. P., Maier, S. F., & Geer, J. H. (1968). The alleviation of learned helplessness in the dog. *Journal of Abnormal Psychology*, 73(3, Pt.1), 256—262.
DOI: 10.1037/h0025831

Seligman, M. E. P., & Groves, D. (1970). Non-transient learned helplessness. *Psychonomic Science*, 19(3), 191—192.
DOI: 10.3758/BF03335546

Seligman, M. E. (1972). Learned helplessness. Annual review of medicine, 23(1), 407—412.
DOI: 10.1146/annurev.me.23.020172.002203 PMID: 4566487

Seligman, M. E. P. (1974). Depression and learned helplessness. In R. J. Friedman & M. M. Katz (Eds.), *The psychology of depression: Contemporary theory and research*. Oxford, England: John Wiley & Sons.

Seligman, M. E. P. (1975). *Helplessness: On depression, development, and death*. San Francisco: Freeman

Seligman, M. E. P., Abramson, L. Y., & Teasdale, J. D. (1978). Learned Helplessness in Humans: Critique and Reformulation. *Journal of Abnormal Psychology*, 87(1), 49—74
DOI: 10.1037/0021-843X.87.1.49 Retrievable from: Semantic Scholar

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Tags: behavior, conditioning, learned-helplessness
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