What explains variability in the mean firing rate across biological neurons? Biological neurons have a trade-off between high information transfer (high firing rate) and energy conservation (low firing rate). One would suspect that the maximization of this function has a single solution, and that the mean firing rate and variability should be similar across all neurons. Yet this is far from the case. Is there a principled computational explanation for this variability?

I am not sure whether the three assumptions on which your question is based are really valid.

(1) Why should a high transformation transfer be linked to a high firing rate? Depending on the role of a single neuron within a group, not firing might carry as much as information as firing.

(2) Energy conservation might not be linked to the behavior of a single neuron, but rather to the organism as a whole. For instance, if the constant firing of a neuron stops your legs from constant (dis-functional) shaking, the energy "wasted" on the firing neuron can lower the energy consumption of the system as a whole.

(3) Although not explicitly stated, your question might suggest that the mean firing rate of a given neuron is relatively constant over time. This is not necessarily the case, as the firing characteristics of neurons are "tuned" over time, depending on its activity. This process is called homeostatic synaptic plasticity and has received much attention recently.

For a review see:
Turrigiano GG. (2008) The self-tuning neuron: synaptic scaling of excitatory synapses. Cell. 422-35.


Can cognitive science improve psychology? I was wondering what your guys thoughts were about cognitive science making unique contributions to improve the methodological and theoretical foundations of psychology?

Can it make unique contributions?
Will it ever be able to replace psychology?
What about the replication crisis of psychology? Does this have an impact on the reputation of cognitive science?

Looking forward to hearing your thoughts.

Answering this question is very difficult without first agreeing what "cognitive science" is (a problem for this very site!). Unlike another answer here, to me, cognitive science is not necessarily about neuroscience methods (that would be cognitive neuroscience). Instead, cognitive science is an interdisciplinary hodgepodge of people doing empirical psychology, computer science, linguistics and philosophy of mind. And I say this as a member of the Cognitive Science Society. Although neuroscience is often involved, cognitive science is much older and historically linked to computing, AI and the cognitive revolution.

It certainly has made, and will continue to make, unique contributions to psychology. One can argue about the overlap between cognitive psychology and cognitive science (to me it is considerable), but theories of information processing from computing, computational models, linguistic theory and many other examples can make more precise predictions which people can verify with empirical data (these people are normally psychologists). This improves psychology which has sometimes suffered from being too vague ("boxology").

Because I see CS as an umbrella including psychology, I don't think it makes sense to think of it "replacing" psychology.

Because CS has often included people doing empirical experiments on human behaviour, the replication crisis certainly has implications (though it may be buffered by it's emphasis on theory). Cognitive psychologists are certainly guilty sometimes, though much of the soul-searching on replications, p-hacking etc comes from experimental social psychology.


Do we know a priori any rules about the world? 1) Is there any set of rules that human beings or, more generally, other sentient living beings know a priori before any learning process?
In other words, do sentient living beings always were born knowing some causal relations about the world?
For instance, a newborn baby may not know that walking from a high place in direction of an edge may result on him falling due to gravity. Maybe he doesn't even know that he can move its arms and he only learns that after performing fortuitously an impulse that generates such action. Maybe he doesn't even know that he must breath in order to survive and he only learns that after feeling the discomfort and pain caused by the lack of oxygen.
As a disclaimer, I'm excluding here tautological logical syllogisms such as the principle of non contradiction and other axioms of logic. I'm also excluding here any synthetic a priori knowledge that can be derived from these (if you believe in synthetic a priori).
2) In the positive case, how complex can these causal relations be (maybe a measure or an undeniably remarkable complex a priori knowledge)?
I'm particularly interested in a priori knowledge about normative judgements mainly related to social mores.

This is a pretty popular research topic!
One good place to start might be with the work of Spelke, she's all over this.
Try this: https://www.youtube.com/watch?v=nNq_a_wgdgQ

If you prefer written words, this paper is a nice broad overview, although note the 2007 publishing date, there's been a fair bit of work since then.
Spelke, Elizabeth S., and Katherine D. Kinzler. "Core knowledge." Developmental science 10.1 (2007): 89-96.


Introductory material on psychophysics with a focus on visual stimuli Is there any introductory-level material available on psychophysics that you can recommend to someone without a background in cognitive sciences? Visual stimuli is the main area of interest.

Edit: Question has been narrowed down in response to comments

I never read any English textbooks on psychophysics, so I cannot help you there. If I wanted to find a good one, I would look at the curricula at some universities and see which books they use or recommend. Such information is often available online.

Beyond a textbook, like user1406647 (+1), I find it enlightening to read classic experiments by the inventors of psychophysics. Their texts are easy to understand without much previous knowledge, and the experiments are simple and foundational for the understanding of the principles of psychophysics. Also, I believe that textbooks only ever give a vague and superficial idea of a field, while confrontation with original texts provides a deeper insight. This is especially true for the presentation of theories: in textbooks they are always abbreviated beyond recognition. Textbooks are good in that they provide a possible structure (e.g. they group authors and theories), delineate historical development, and summarize critique. They are like maps: you'll have to do the walking yourself, but you know where you might find the most spectacular sights.

That said, I want to give some few examples that I found especially basic. Any one of these or similar articles will give you an understanding of what psychophysics is about. A good textbook should give you some references to more such experiments.

Charpentier on the Size-Weight-Illusion:
Charpentier, M. A. (1891). Analyse expérimentale de quelques éléments de la sensation de
poids. Archives de Physiologie Normale et Pathologique. Cinquième Série, 3, 122-135. Available online at http://gallica.bnf.fr/ark:/12148/bpt6k4327622/f125.image
An English translation by David J. Murray and Robert R. Ellis has fortunately been archived at http://www.oocities.org/robertellis600/charp.htm
Background information on Charpentier's article is provided in:
Murray, D. J., Ellis, R. R, Bandomir, C. A., & Ross, H. E. (1999). Charpentier (1891) on the size-weight illusion. Perception & Psychophysics, 61, 1681-1685. doi:10.3758/BF03213127
Plateau on Averaging of Achromatic Colors:
Plateau, J. (1872). Sur la mesure des sensations physiques, et sur la loi qui lie l'intensité de ces sensations à l'intensité de la cause excitante. Bulletins de L'Academie Royale des Sciences, des Lettres et des Beaux-Arts de Belgique, 2me Sér., 33, 376-388.
An English translation by Janet and Donald Laming has been published as:
Laming, J., & Laming, D. (1996). J. Plateau: On the measurement of physical sensations and on the law which links the intensity of these sensations to the intensity of the source. Psychological Research, 59, 134-144. doi:10.1007/BF01792434
The experiment has been replicated and discussed in:
Heller, J. (2001). Mittenbildung bei achromatischen Farben: Das klassische Experiment von Plateau. Zeitschrift für Experimentelle Psychologie, 48, 259-271. doi:10.1026//0949-3946.48.4.259
I'll update this answer with more examples when I have the time.


Is what psychologists define as subconsciousness proven in neuroscience and can the psychological subconsciousness be visualized by neuroscientists? We read phrases like

The subconsciousness makes up 90% of our brain.
The subconsciousness makes up 95% of our brain.
The subconsciousness can be influenced by hypnosis.

I have yet to see a study in neuroscience that picks the topic up. There seems to be no proof of its existence other than a psychological crutch to explain behaviour.

People like Bruce Lipton try to connect neuroscience to psychology and do not convince in doing so.

Is what psychologists define as subconsciousness proven in neuroscience and can the psychological subconsciousness be visualized by neuroscientists? I am alluding to pictures or video of the images perceived...........

The vast majority of neural processes (and their associated mental processes) in the brain are subconscious (or unconscious), i.e. we are not consciously aware of them and cannot consciously control them. Yet, without these subconscious processes, we will not be able to live as we do now – we will have to spend an incredible amount of time and effort to consciously control all the processes that are naturally subconsciously controlled now. As a matter of fact, we will not be able to consciously do such tedious yet demanding tasks well, and we will die.

All neural processes except the final-stage sensory perception neural processes and the highest cognitive neural processes are subconscious. The subconscious neural processes are in all parts of the brain:

Brainstem and autonomic system. For example, neural processes that control breathing, heart contraction, pressure in the arterial and venous systems, body temperature, sleep-wake cycle, secretion of various body fluids (sweat, tear, saliva, gastric juice, etc.), secretion of various hormones, various reflexes (pupillary light and accommodation reflexes, optokinetic reflex, vestibulo-ocular reflex, etc .), homeostasis of various blood constituents, etc.
Cerebellum. For example, neural processes that control contraction & movement of hundreds of millions of muscle fibers of various agonist and antagonist muscles for balance and accuracy in walking, writing, speaking, playing various sports, playing various musical instruments, etc.
Deep cerebral nuclei. For example, neural processes that control the tone of your trunk muscles (when sitting, standing, walking, etc.), emotion (*1), formation, storing, and retrieval of memory (*2), etc.
Cerebral cortex. For example, neural processes that perform early-stage sensory perception (*3), early-stage language functions (*4), some stages of decision, some forms of thinking (*5), etc.

And, if you include spinal cord, the majority of their neural processes are subconscious too.

N.B.

*1. That's why we can't completely control our emotions at will: we can't get out of anger, sadness, depression, etc. or get into any emotion we want instantly at will, because they are partly controlled by subconscious neural processes. Also, we will not be able to have any emotion even if we try to if the subconscious neural processes (in the amygdala and other nuclei in the limbic system) for emotion are impaired (such as in various apathy disorders: Alzheimer’s disease, Parkinson’s disease, fronto-temporal dementia, etc.)

*2. That's why you can't memorize new events or recall past events, even if you try, if the subconscious neural processes (the hippocampus and other nuclei in the limbic system) that form, store, and retrieve memory are impaired.

*3. That's why we can't consciously see in colors (achromatopsia), can’t recognize familiar faces (prosopagnosia) (including one’s own face), or can't recognize what the object is (visual agnosia) if the subconscious processes that process color, object identification, or face identification are impaired.

*4.That's why we can't understand what people say even if we hear them clearly (sensory dysphasia) or can't understand what the text in the book means even if we see it clearly (alexia) if the subconscious neural processes that processes the meaning of the sound or of the image is impaired.

*5. See more details in the references below.

References.
General, basic information about unconscious processes in the brainstem, autonomic nervous system, cerebellum, and deep cerebral neuclei (basal ganglion, thalamus, amygdala, etc.) can be found easily by searching the internet.

Some of the more in-depth, interesting articles about this matter are as follows (and more references can be found inside these articles):

Bargh JA, Morsella E. The Unconscious Mind. Perspect Psychol Sci. 2008 Jan;3(1):73–79. DOI: 10.1111/j.1745-6916.2008.00064.x.
Dehanene S. Fathoming unconscious depths. In: Consciousness and the brain. Penguin Books. 2014. New York, New York, USA. ISBN 978-0-670-02543-5, 978-0-14-312626-3. p 47-88.
Dijksterhuis A. First neural evidence for the unconscious thought process. Soc Cogn Affect Neurosci. 2013 Dec; 8(8): 845–846. doi: 10.1093/scan/nst036.
Dijksterhuis A, Strick M. A Case for Thinking Without Consciousness. Perspect Psychol Sci. 2016 Jan;11(1):117-32. doi: 10.1177/1745691615615317.
Hallett M. Volitional control of movement: The physiology of free will. Clin Neurophysiol. 2007 Jun;118(6):1179–1192. DOI: 10.1016/j.clinph.2007.03.019 PMCID: PMC1950571 NIHMSID: NIHMS24077.
Horga G, Maia TV. Conscious and unconscious processes in cognitive control: A theoretical perspective and a novel empirical approach. Front Hum Neurosci. 2012; 6:199. doi: 10.3389/fnhum.2012.00199.


What is the best way to turn EEG scans in to 3D images? I'm looking for the best way to turn standard EEG scans into 3D images of activity in the brain over the time of scanning, for example like the Glass Brain images or even connectome-style images.

I have experience of collecting EEG data and basic experience of EEG analysis using the SPM package for MATLAB, but this didn't include creating a 3D image.

Is there capability to create this using SPM or perhaps another add on or even other software entirely that I can access?
Alternatively, does anyone know of any service which would do this for me?
I work for for a technology company, not as part of a testing lab or affiliated to a university, so don't have access to these sorts of labs and expertise.

By 3D image, I assume that you want a projection of the topographic map onto a 3D model of the head. For an accurate resolution, you would need to have acquired the position of the EEG channels on the head as well as the shape of the participant's head. However, this kind of data is not often acquired.

The next best solution is to use an existing model of the channel position for your EEG system on a template head. The head plot function in EEGLAB can do that: http://sccn.ucsd.edu/eeglab/allfunctions/headplot.html

Transferring your files from SPM format to EEGLAB format should be quite straightforward. You can find solutions to this problem on both the EEGLAB and SPM mailing lists.


What indicates an extreme worry about privacy? Some persons pretends that to be curious of other's people life facts is disrespectful.

I imagined that this belief comes from coherence and a projection on others of our worrying about privacy.

I'm strongly worried about my privacy => others could be as well => curiosity is disrespectful

Is this hypothesis correct?

I'm by no means an expert or qualified, but here's my thoughts.
I believe there are a few factors at play:

Our Privacy

The first is the perception that the information carries some threat to their lifestyle or reputation, e.g. an adult who views pornography or a cheating spouse, for both of whom this causes that initial concern of the threat of exposure (and we may over-estimate their impact upon exposure as a form of impact bias).

Second, narcissism: they're worried their actions could be considered damaging to their image and believe that those who invade their privacy (a government / a social network selling aggregate topic stats to marketers, etc.) would take great delight in exposing their behaviour. Of course they wouldn't, but people generally like to think their own lives are of importance to everyone, and so why wouldn't their "important" secrets be of importance to everyone else?

Others' Privacy

First I'll throw in that the person may remember the last time they were burnt by their privacy being invaded by others (such as malicious gossip), which may serve as a negative reinforcement to not infringe on others'. You remember the last time and how much it hurt you and don't wish to knowingly inflict that on someone else, especially for no personal gain.

There is also the thought that if we do a good deed that others will reward us for it...or if we deem ourselves to have done something selfless, we derive gratification from it. This is also closely linked to narcissism. I read something ages ago that inferred there is never a truly selfless act, as we often do it to feed our ego.

If legislative changes are made to protect privacy generally (e.g. social networks' usage of private messages are tightly controlled), then we also could benefit from this, so there is also potentially some selfish gain in concern over other people's privacy, and we can project how we are annoyed at a particular company doing something with our data on "behalf of a friend".

Finally, if we believe strongly that our own "privacy" is important (when in reality most people are just referring to morally questionable behaviour they would like to suppress), then we also see others' as just as important as some way to justify that our own belief in the protection of our privacy is founded. A "bias blind spot" and "confirmation bias" appear in the list of cognitive biases.


How is Pain Subjective and Different from Nociception So pain is the sensory feeling that tells indiviual that something bad at some part of the body has happened. What I fail to understand is how is pain subjective? If we have touch receptors in the body we can technically all feel hyptactic simulation, why this cannot be said about pain.
In this article it is mentioned:

pain is different from nociception, which is the ability to respond to damaging stimuli.  All organisms have nociception.  Even bacteria can move away from harmful environments such as high pH.  But not all animals feel pain.

Question: How is pain subjective? Why nociception isnt considered pain?

Q: How is Pain Subjective and Different from Nociception?
A: Pain is not nociception because their definitions are different. The usual definitions are like this:

Nociception refers to the peripheral and central nervous system (CNS) processing of information about the internal or external environment, as generated by the activation of nociceptors. Typically, noxious stimuli, including tissue injury, activate nociceptors that are present in peripheral structures and that transmit information to the spinal cord dorsal horn or its trigeminal homologue, the nucleus caudalis. From there, the information continues to the brainstem and ultimately the cerebral cortex, where the perception of pain is generated.  Pain is a product of higher brain center processing … (1)

Or
“Nociception (also nocioception, from Latin nocere 'to harm or hurt') is the sensory nervous system's process of encoding noxious stimuli. In nociception, intense chemical (e.g., cayenne powder), mechanical (e.g., cutting, crushing), or thermal (heat and cold) stimulation of sensory nerve cells called nociceptors produces a signal that travels along a chain of nerve fibers via the spinal cord to the brain.1 Nociception triggers a variety of physiological and behavioral responses and usually results in a subjective experience (or perception) of pain in sentient beings.”(2)
That is, nociception is defined to be the processing of noxious stimuli, which involves several levels of processing, but pain is defined to be the perception of the result of nociception processing. As there are many factors that can affect nociception at each level of processing, such as the pain control mechanism (e.g. the pain gate control) in the spinal cord and brainstem, analgesics, and even the mood of the subject, the pain perception can be altered/modified, and the final pain perception can be different even if it occurs in the same individual and from the same noxious stimuli. Also, because these factors are different among different subjects, the final pain perception in each individual is subjective – depending on various factors in each subject and different among different subjects even if it occurs from the same noxious stimuli.
For example:

When your shin hits something hard and you feel pain there, if you stroke or massage the injured shin lightly, you’ll feel better with less pain – this is because the pain is modified by the pain gate control or other pain control mechanisms by the touch sensation. (3,4)

In a person who has a spinal cord transection with a loss of all sensations and voluntary movements of the legs, if you prick his foot, his foot will involuntarily jerk away from the prick, which means nociception is still being processed, but you won’t feel any pain because the pain perception in the brain does not occur (due to the spinal cord transection).

Alice has been given a flu shot in her arm, but she is a strong person and is in a good mood, so she feels little pain in her arm. On the contrary, Bob has been given a flu shot with the same needle size and ease of injection, but Bob is an irritable person and already in a bad mood, so he feels that the pain from the shot is very severe. So, the pain perceived from the same noxious stimuli is different among different subjects, depending on various factors in each subject.

Therefore, the pain is different from nociception and is subjective.
References:

National Research Council. 2009. Mechanisms of Pain In: Recognition and Alleviation of Pain in Laboratory Animals.  Washington, DC: The National Academies Press. https://doi.org/10.17226/12526.

Wikipedia. Nociception

Nachum Dafny.Chapter 8: Pain Modulation and Mechanisms. Neuroscience Online. The University of Texas Health Science Center at Houston (UTHealth).

Wikipedia. Gate Control Theory


What does the following sentence mean? I don't understand what they are referring to when they say "saturating concentrations" and "basal conditions"? Here is the quote:
"Because BH4 is not present in saturating concentrations under basal conditions, it is crucial in regulating TH activity."
This is from Fundamental Neuroscience, page 121.

I will rewrite the sentence another way that preserves what a believe is the intended meaning:

There is little enough BH4 under normal conditions such that levels of BH4 are important for TH activity.

BH4 is an enzyme cofactor; in this context they're talking about it used with tyrosine hydroxylase (TH) to make a precursor (L-DOPA) to dopamine.
If there was so much BH4 available at basal (normal) conditions that adding more doesn't speed up TH activity, we can say it's saturated. In that context, BH4 changes don't really regulate TH activity (unless they are huge changes that bring it well below the 'saturated' level).
The sentence you quoted is saying this isn't the case. BH4 isn't present at saturated levels, so you can influence TH activity (and therefore synthesis of L-DOPA) by influencing BH4 concentration.


Diagnosis for consistently preceiving mild displeasure as personal threats? I'm aware the site does not accept self-help questions, but I think this one can be answered in a situation-independent way. So

Is it possible for someone to exaggerate mild displeasure (justfiable or unjustifiable through social norm) as personal threats?
And what does it mean?

Short answer
Paranoid personality disorder and social anxiety disorder come to mind.

Background
Perhaps you are after paranoia, which is thinking and feeling as if you are under threat even though there is no (or very little) evidence that you are. Paranoid thoughts can also be described as delusions. Paranoid thoughts can be exaggerated suspicions, e.g.., someone made a negative comment about you once, and one inflates that rather irrelevant remark to a full-blown hate campaign.
Thanks to r0berts' commentary below, I wish to add that, according to the DSM-IV-TR, paranoia in itself is not a diagnosis. Instead, it is diagnosed in the form of paranoid personality disorder, paranoid schizophrenia (a subtype of schizophrenia), or the persecutory type of delusional disorder. paranoid personality disorder may be what you are after in specific:

  Paranoid personality disorder is generally characterized by a
  pervasive distrust and suspiciousness of others. Sufferers often
  believe that other people’s motives are suspect or even malevolent.

Paranoid schizophrenia is characterized by predominantly positive symptoms of schizophrenia, including delusions and hallucinations. Without going into detail, schizophrenia is probably not what you are after.
People with persecutory type of delusional disorder believe that they (or someone close to them) are being mistreated, or that someone is spying on them or planning to harm them. Likely also not what you are after.

Another disorder that comes to mind is anxiety disorder, and specifically

  social anxiety disorder, or social phobia. This is
  characterized by overwhelming worry and self-consciousness about
  everyday social situations. You fixate about others judging you or on
  being embarrassed or ridiculed.


Are there scientific alternatives to Neuro-Linguistic Programming (NLP)? According to these answers 1, 2 and to wikipedia, NLP seems to be a pseudoscience, which has shown no real effectiveness, and so on.

Are there scientific proved alternatives to NLP?

In general positive psychology, coaching, and counselling are all fields that endeavour to help people achieve their potential. All these areas have scientific literature built around them. That said, there is a degree to which coaching and counselling are practical skills. Most psychologists aspire to follow the scientist-practitioner model. That said, specific practitioners may vary in the degree to which they follow this model versus using more intuitive approaches.


Have EEG signals in auditory speech perception task have ever been analyzed for correlation with auditory stimuli itself? This can be useful for getting a better grip on understanding the link between actual stimuli, brain processing, and EEG data.

Extensively. Most prominently, recently, by David Poeppel, Oded Ghitza and Anne-Lise Giraud, in a series of papers. They've, to be precise, mostly focused on MEG  correlations with the filtered speech amplitude envelope. Areas around the auditory cortex track it fairly well it seems. There is still much debate about what this means and where it comes from, but it's been discussed. Example here.

There is also the spectrotemporal response function, which is a somewhat generalized concept and mostly employed in an sEEG context. Example here. It looks like this:


What is the difference between Psychology, and Thymology? I understand Thymology to not merely be a synonym, but to be a branch or area of Psychology, however I am at a loss of how to properly distinguish the two.

What distinguishes Thymology from Psychology in general?

Thymology is an historical conjecture on why someone thought the way they did. For example, why did Herbert Henry Asquith take his country to war in 1914. What thought processes went into that decision. The decision is often made to seem inevitable given preceding experiences. There is a school of thought that would lump this study alongside other accounts of history and journalism, in that they fall into the trap of searching for causes for things that are just as likely to be caused by randomness (i.e. perhaps he went to war because the decision was made shortly before lunch and he was hungry and irritable, rather than because of a neat causal explanation).

Psychology is the general study of mind and behaviour in general, largely in the present, and tested scientifically with controlled experiments, simulations, statistical inference, and qualitative research.


DSM and references to ICD I am still studying and where I extensively use the DSM whilst writing essays etc. for my coursework, a question has arisen with regard to referencing the International Statistical Classification of Diseases and Related Health Problems (ICD) whilst researching, and whilst answering a question within Cognitive Sciences.  Providing the answer raised this question when referencing the ICD codes used in the DSM.

Those familiar with 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) will know that with information on each mental health disgnostic criteria, there are ICD codes at the top, which are ICD-9 codes followed by the now compulsory ICD-10 codes in brackets.  Whilst in my essays etc., just like in the DSM-5, I reference both ICD-9 and ICD-10 codes, however all HIPAA-covered entities had to transition from using ICD-9 codes to using ICD-10 codes back in late 2015.

The problem arises for me when looking in the ICD for the codes referenced in the DSM.  I'll give some examples here.

In order for me to answer the question, I referenced DSM diagnostic criteria for Somatic Symptom Disorder, Illness Anxiety Disorder and Body Dysmorphic Disorder (BDD).

For Somatic Symptom Disorder, in the DSM it references ICD-10 code F45.1 which in the ICD, that code is for Undifferentiated Somatoform Disorder, however as I highlighted in my answer, F45 which is the header of that section of codes refers to Somatoform Disorders.
When looking at Illness Anxiety Disorder, the DSM references ICD-10 code F45.21 which doesn't exist.
When looking at BDD, the DSM references ICD-10 code F45.22 and when you look in the ICD, again there is no such code, however there is F45.2 which refers to Hypochondriacal Disorder which in turn references BDD as a Hypochondriacal Disorder.

On page 23 of DSM-5 - under Coding and Reporting Procedures, which is within the Use of the Manual section - it indicates that the ICD codes are typically used by institutions and agencies for data collection and billing purposes and they were established by WHO, the U.S. Centers for Medicare and Medicaid Services (CMS), and the Centers for Disease Control and Prevention's National Center for Health Statistics to ensure consistent international recording of prevalence and mortality rates for identified health conditions.

Am I missing something when looking at the ICD publication to look the diagnoses up under the ICD-10 codes or am I looking at things in the wrong way?

There is this 2009 article on the APA website (The APA are the writers of the DSM)

It states that

  There is widespread sentiment that it is not helpful to the field to
  have two separate classification systems for mental disorders. [However], Many
  important distinctions between the two systems remain.

The article also mentioned that Geoffrey Reed (WHO psychologist) said:

  The American Psychiatric Association can really be credited with a
  revolution in psychiatric nosology with the publication of DSM-III by
  introducing a descriptive nosological system based on co-occurring
  clusters of symptoms,...
  The ICD is produced by a global health agency with a constitutional
  public health mission, while the DSM is produced by a single national
  professional association.WHO's primary focus for the mental and
  behavioral disorders classification is to help countries to reduce the
  disease burden of mental disorders. ICD's development is global,
  multidisciplinary and multilingual; the primary constituency of the
  DSM is U.S. psychiatrists.The ICD is approved by the World Health
  Assembly, composed of the health ministers of all 193 WHO member
  countries; the DSM is approved by the assembly of the American
  Psychiatric Association, a group much like APA's Council of
  Representatives.The ICD is distributed as broadly as possible at
  a very low cost, with substantial discounts to low-income countries,
  and available free on the Internet; the DSM generates a very
  substantial portion of the American Psychiatric Association's revenue,
  not only from sales of the book itself, but also from related products
  and copyright permissions for books and scientific articles.

The article also says

  There was very little international participation in the DSM-III, but
  at the time it may have been impossible to make such a big shift at
  the international level, he explained. As a result, DSM-III and ICD-8
  (the version in effect at the time) were quite different from one
  another but as the descriptive phenomenological approach to diagnose
  mental disorders became dominant, the DSM and ICD have become very
  similar, partly because of collaborative agreements between the two
  organizations.

The article asked if the DSM will be superseded by the ICD?

It said

  There is little justification for maintaining the DSM as a separate
  diagnostic system from the ICD in the long run, particularly given the
  U.S. government's substantial engagement with WHO in the area of
  classification systems. But, said Reed, "there would still be a role
  for the DSM, because it contains a lot of additional information that
  will never be part of the ICD. In the future, it may be viewed as an
  important textbook of psychiatric diagnosis rather than as the
  diagnostic 'Bible.'"

As there is more information in the DSM that will never be part of the ICD, plus, due to the fact that the DSM is the goto book for psychiatry, it is the DSM's criteria which needs to be followed when making psychiatric diagnoses.  The ICD codes in the DSM should just be used for the purposes they have been designed for, which as mentioned in the DSM on page 23, they are for data collection and billing purposes and for health statistics to ensure consistent international recording of prevalence and mortality rates for identified health conditions.


Analysis according to Jung's Psychological Types Recently I read Jung's Psychological Types out of self-questioning. I would like to analyze myself in such a fashion more "professionally", however I do not profess to be able to do that myself, having no prior education and training in psychology. I have already done the MBTI test, but after reading Jung's book, I realize that the test is not exhaustive.

My question is - which types of therapists or specialists normally perform these analyses? Do some psychologists base their analysis on Jung's theory? Is it possible to ask "just" for a personality analysis based on Jung's Psychological Types? Or is this theory just an auxiliary method, and does not play as an approach per se?

If you are simply interested in how your personality would be construed within this specific psychoanalytic framework out of pure curiosity, I'm sure one of those Jungian psychanalists Chuck Sherrington mentioned would be tell you something about it (they get paid for it, after all). However, I think they would use the MBTI - that seems to be the only real implementation of a test of Jung's psychologcal types. Furthermore, I feel compelled to caution against personality type tests such as the MBTI from a scientific point of view, because they seem to have little to no empirical basis [1]. There are better personality tests out there. In fact, I would caution against psychoanalytic approaches in general, because they are hardly scientific. [2] So, in my personal opinion, if you are just curious, go for it. If, however, your purpose is anything more than entertainment, steer clear.

[1] Pittenger, David J. "Measuring the MBTI… and coming up short." Journal of Career Planning and Employment 54.1 (1993): 48-52.

[2] de Maat, Saskia, et al. "The current state of the empirical evidence for psychoanalysis: a meta-analytic approach." Harvard review of psychiatry 21.3 (2013): 107-137.


Is there evidence that brain and mind are separate? I've heard countless discussions about whether or not the mind is separate from the brain, but they have all been philosophical.

I am looking for peer-reviewed studies that suggest the mind is not just a by-product of the brain, as I feel this is quite an extraordinary claim.

Are there any such studies?

Another approach to this issue is to consider whether this kind of reductionism ("mind is just a by-product of the brain") is useful. Strictly speaking, architecture is "just a by-product of physics and materials science", but there are phenomena that are usefully described at the level of architecture and would not be well-captured by the atomic and molecular properties that underlie them. The same holds for the mind and brain: we can study the neural correlates of psychological phenomena and these studies are sure to help us understand those phenomena, but they are not logically equivalent. This view has been articulated by many people, here is one (peer-reviewed) example: Miller, G.A. & Keller, J. (2000). Psychology and Neuroscience: Making Peace. Current Directions in Psychological Science, 9(6), 212-215. You don't need to be a dualist to hold this view, just to understand that phenomena can have different levels of analysis.


How are the logical and mathematical skills of people with ADHD? How does rationality and the logical thought processes of those with and without ADHD compare? Please explain the source of the differences. Are the differences thought to be caused by dopamine, serotonin, or norepinephrine? Or is there some other neurological explanation?
How do the math skills of those with ADHD compare to others? As above, please explain in detail from a biochemical perspective.

How do the rationality and logical thought processes those with and without ADHD compare? Please explain the source of this difference. Is the difference thought to be caused by dopamine, serotonin or norepinephrine or some other neurological explanation.

ADHD is typically associated with a reduction in dopamine and/or norepinephrine. Though the two neurotransmitters are similar on a structural level, norepinephrine is associated with vigilant attentiveness, whereas dopamine is associated with cognitive alertness. ADHD is commonly associated with a reduction in dopamine activity, and since norepinephrine is synthesized by dopamine, there are typically deficiencies in both.

In the brain, cortical norepinephrine (NE) is released during attentional patterns so that learning can commence and be enhanced. When we receive information that goes against sensory information (or what we had previously thought true), NE levels 'spike' and then subside once the information is sufficiently integrated. With lower levels of NE, it is harder to pick up on information, and thus the information may not be consolidated and 'learned'. NE also affects memory for facts and specific details in those with ADHD, and thus it can be harder to recall factual information when necessary. You can guess what happens next, as factual information is crucial for building a 'bank' of information in the brain.

Rationality (by definition) factors in how much information is available, and uses it to maximize expected utility. Those who suffer from ADHD have less information available to them, as they do not pick up on information in the way that the average person might. It is not that they are less capable of rational thought -- they simply have less information to make informed, rational decisions.

ADHD is occasionally associated with lateral thinking, which is a method of problem-solving that relies on creative thinking moreso than step-by-step logic. However, I have found no evidence in scientific literature that suggests a link between the two.

  How do the math skills of those with ADHD compare to others? As above please explain in detail from a biochemical perspective.

It depends on how salient math is to the individual. Albert Einstein and Paul Erdős were both considered to have ADHD, and nobody would doubt their math skills. :)

Learning disabilities do tend to work in conjunction. Of those with arithmetic learning disabilities, a quarter of them have ADHD, and up to 31% of those with ADHD are reported to have math learning disabilities. Inattention is typically associated with mathematical learning, as failure to learn to automize computational skills leads to calculation error and slower internalization rate. Children with ADHD typically have problems with fluency of calculation. In other words, it takes longer for them to make calculations internally, and this does not appear to normalize with age. This is because holding information in your head is an essential component of making mental calculations, and this is something that those with ADHD struggle with.

Interestingly enough, math performance in ADHD sufferers has shown to improve with a) more computational practice (so that mental math becomes more 'intuitive'), and b) music playing in the background while attempting to solve math problems. You can read more about this in the article I linked to above.


What are the key examples of the use of computational methods in the study of biological neural networks? In an upcoming postdoc, I'm going to be looking through biological neural network data in the hopes of finding some interesting "patterns".  I'm coming at this field from a mathematics/computer science point of view, and am quite new to the biological side of things.  I'm hoping that by looking at some examples in which computational methods were successfully used in understanding biological neural networks, it might help me understand more about what I should be looking for, and what approaches are likely to be successful.

  Question:  What are some key examples in which computational methods were used on biological neural networks to gain important insights into these networks?

I'd like to add to Chuck's excellent answer; the computational approach is very well-represented in neuroscience, and actually involves a large number of very heterogeneous methods.  Thus, a very different set of neuroscientists and examples have sprung to mind for me.

To my mind, the best single example of the utility of a computational approach to interpreting neural data is the reward prediction error hypothesis of dopamine function.  Early investigations in machine learning led to the development of the temporal difference reinforcement learning algorithm.  Subsequently it was noticed, by Wolfram Schulz, that the pattern of firing in dopaminergic cells appeared to closely correspond to what would be expected of a temporal difference error signal - the very core of this form of reinforcement learning. Subsequently, similar reinforcement learning algorithms (e.g., Q-learning) have been applied to a variety of neural data - albeit at the much coarser scale of fMRI - and provided a variety of evidence that is strongly supportive of this hypothesis. This work has been absolutely crucial to progress in the last 10-15 years in cognitive and systems neuroscience.

The second example that springs to mind also pertains to dopamine; in this case, the utility of the computational approach was in understanding the pattern of effects produced by release of dopamine, rather than in characterizing the pattern of dopamine release itself.  At the cellular level Jeremy Seaman's work is a great example of this approach; he has used Fisher discriminant analysis and other multivariate techniques to better characterize multi-unit activity recorded in prefrontal cortex, under various dopamine conditions.  Ultimately his work has been the primary computational approach contributing to what is now the modal understanding of dopamine's effect in the prefrontal cortex, which is to enhance signal to noise ratio.

A third example has to do with the application of graph theory to neural networks, and in particular our understanding of small-world connected graphs.  The implication of this work for neuroscience was not lost on the mathematicians that originally pursued this line of work, but its actual utility for neuroscience has been most famously demonstrated by Olaf Sporns in understanding what is coming to be called the "connectome" - that is, the graph of structurally- and functionally-connected neural systems.  Although this is still an active line of research, small-world connectivity appears to be a ubiquitous feature of cortex.

I would be remiss not to mention the work of a large group of researchers trained in the "parallel distributed processing" or connectionism tradition, including Matt Botvinick, Jon Cohen, Michael Frank, Ken Norman, Yuko Munakata, Randy O'Reilly. There are too many excellent examples from their work to name, but all of these researchers have used behavioral and neural data to build neural network models of cortical and subcortical processing, at varying levels of biological detail; validated these models in terms of their fit to existing behavioral and neural data; and used these models to derive predictions that have subsequently been tested using a variety of approaches. The following is a woefully incomplete, but at least representative, list of the progress made by these researchers: the discovery of parallels between the dimensionality-reduction or "abstraction" techniques that can be useful in reinforcement learning to cortical processing (in the case of Matt Botvinick); the discovery of parallels between the exploration/exploitation dilemma in reinforcement learning and the function of the locus coereleus/norepinephrine system (in the case of Jon Cohen); the understanding of fine-grained functional consequences of differences in dopamine receptor subtypes, as well as prefrontal/striatal interactions (in the case of Michael Frank), the discovery of the large-scale consequences of cellular-level long-term depression and potentiation phenomena for hemodynamic patterns in memory tasks (in the case of Ken Norman), the discovery of the role of prefrontal inhibitory neurotransmission in tasks requiring "selection" of information under competition (in the case of Yuko Munakata), and the discovery of the computational underpinnings of the tri-partite division of labor between hippocampus, posterior cortex, and prefrontal cortex (in the case of Randy O'Reilly).  Jay McClelland, David Rumelhart, David Seidenberg, Geoff Hinton, and many others laid the groundwork for much of this progress, although their contact with detailed neural phenomena was more limited than that made by their trainees (and their trainees' trainees), above.

I would conclude by seconding Chuck's suggestion to do a PubMed search.  Your question is too broad for a comprehensive answer conveyed in anything shorter than a book!


List of affective states for a study? I am putting together a study that attempts to assess whether people assign particular affective or emotional states to images--specifically, animated GIFs. Is there a "standard" list of emotional states that has been used in research before, or that tends to be favored by researchers who study emotions? I'm considering something like Plutchik's three-dimensional circumplex model, but I didn't know if there was something else that tended to be more favored.

There are a range of "adjective checklists" that have been developed to assess affective states, personality traits, or characteristics of individuals. Two of the most widely cited measures are the Multiple Affective Adjective Check List (MAACL) and the Multiple Affective Adjective Checklist-Revised (MAACL-R) (Zuckerman & Lubin, 1965; Zuckerman & Lubin, 1985). Although the actual MAACL-R manual may require purchase, lists of the affective items are available in other publications (Gotlib & Meyer, 1986).

Clinically, I have used the How Do I Feel Right Now? chart for clients who have difficulty identifying and naming their emotional states (http://blogs.oregonstate.edu/careerservices/2012/11/30/emotional-intelligence-what-is-it-and-why-do-employers-want-emotionally-intelligent-employees/).

Other sources of emotion lists in the field of psychology include:

Shaver and colleagues have a heavily cited paper on types of emotions (1987)
The Geneva Emotional Music Scale (Zenter, Grandjean, & Scherer, 2008)

Gotlib, I. H., & Meyer, J. P. (1986). Factor analysis of the Multiple Affect Adjective Check List: A separation of positive and negative affect. Journal Of Personality And Social Psychology, 50(6), 1161-1165. doi:10.1037/0022-3514.50.6.1161

Shaver, P., Schwartz, J., Kirson, D., & O'connor, C. (1987). Emotion knowledge: further exploration of a prototype approach. Journal of Personality and Social Psychology, 52(6), 1061.

Zentner, M., Grandjean, D., & Scherer, K. R. (2008). Emotions evoked by the sound of music: Characterization, classification, and measurement. Emotion, 8(4), 494-521. doi:10.1037/1528-3542.8.4.494

Zuckerman, M., & Lubin, B. (1985). Manual for the MAACL-R: The Multiple Affect Adjetive Check List Revised. Educational and Industrial Testing Service.

Zuckerman, M., & Lubin, B. (1965). The Multiple Affect Adjective Checklist (MAACL).


What are the benefits of giving feedback to subjects during a discrimination task? Context

I am planning an experiment where the subjects would need to determine the language of the stimulus after listening to it once, given two alternatives, L1 or L2.
In total I have 500 trials separated in 5 blocks.

Problem

One of my supervisors insists that I have to give the subjects a feedback immediately after they made the choice ("because the experiment is boring"), and the other one says I should not give them any feedback at all ("they get payed for this, they have to suck it up").

I, for myself, think that maybe giving them scores after the end of a 5-minute block would be helpful to support their motivation and give a little more of motivation for them to concentrate on the following block.

Question

Does anyone here have experience with giving feedback to subjects during the experiment?

Short answer
Giving subjects feedback may affect their performance over time because of learning effects. The choice of giving feedback may be far less trivial than subjects getting bored yes or no. And quite frankly, subjects will get bored after a 100 trials, let alone 500, feedback or no feedback...

Background
You have to be aware that subjects can show learning effects in speech tests (De Jong et al, in press). I am unaware of the specific task you give them, but perhaps below answer will help you make a rational decision on this.

Procedural learning affects the way people perform because they may get better in the task, simply because they have to learn how the task works ('Oh wait, the trial starts already!' 'Oh wait, where was that answer button again?' 'Oh wait, what was the green button for again?'). If subjects show procedural learning effects, they will get better over time. This is oftentimes regardless of whether you give any feedback; subjects simply need to 'get the hang of it'.
Conceptual learning will affect the performance too. This type of learning is strongly affected by whether you give them feedback. For example, if your subjects are unfamiliar with the languages and you are not providing them feedback then they will never learn them. On the other hand, when for example they hear words from a closed set and each word is repeatedly presented, and the experimenter provides the correct answer ('This trial you heard senorita and that is Spanish and means female' or whatever) and the subjects repeatedly hears this word then for sure at a certain point they will learn from feedback that it is Spanish. However, without any feedback they will never learn it.

Even feedback after 5 minutes may affect their performance ('Oh I'm doing great, I can probably relax a bit'). In my opinion, subjects should never be given feedback, not until, perhaps, after the entire experiment is over.

Reference
- De Jong et al., Ear & Hearing, in press


Is there a mental illness that almost completely stops you from thinking? I know the title seems insane, and this is most likely impossible, but is there a mental illness that almost stops a person from thinking? By thinking I mean the "talking in your head" thing. I'm not looking for a mental illness that makes them unconscious, but rather a mental illness that keeps them conscious and almost stops them from thinking. I have been saying this a few times, but I feel like it's false, since thinking is a person can't stop thinking if they are alive and conscious(right?). A more realistic question is: "is there a mental illness that causes one's thinking abilities to severely decline?"

Thinking is mainly supported by the frontal lobes (although the ARAS – the Ascending Reticular Activating System – is essential for its arousal and other cortical areas are essential for its sensory inputs and other associative functions, such as language, spatial orientation, and emotion, which are closely associated with thinking). So, anything that affects the frontal lobes can affect the thinking.
But frontal lobes never stops function if one is still conscious – neurons in the frontal lobes will keep firing as long as  there’s a stimulation from the ARAS. So, to literally stop thinking (or all neurons in the frontal lobes stop firing) in still-conscious people is impossible.
However, frontal lobes can be interfered to the degree that the thinking is significantly impaired or retarded and the person seems to stop thinking. This can happen in a varieties of conditions, such as:
Psychological: severe emotional overload (e.g., by a sudden loss of something so precious, an unexpected devastating event, or an overwhelming rage), schizophrenia in some stages (e.g. catatonic stage), severe depression
Pharmacological: overdosage of antipsychotic, sedative, or other psychoactive drugs
Pathological:

all metalbolic derangements (hypoglycemia, hyponatremia, hypercalcemia, etc.)
some medical conditions (hypothyroidism, hypocorticolism, hypothermia, etc.)
frontal lobes disorders: frontal lobe tumor, infarction, hemorrhage, encephalits, dementing diseases
other causes: post- cerebral contusion, post-ictal stage

At some stages of the above conditions, either before the patients lapse into coma or after they emerge from coma, the patients will appear dazed, muted, unable to think, and unable to respond. That is, apparently, they seem to stop thinking in these conditions.
References:

Wikipedia. Frontal lobe

WebMD. What Is Encephalopathy?

Roger F Butterworth. Chapter 38. Metabolic Encephalopathies. Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition.

Wikipedia. [Delirium](https://en.wikipedia.org/wiki/Delirium


Active Learning vs. Engaged Learning I have seen both of these in different research publications, but after searching for a while, I was not able to find the difference. I'll appreciate it if you explain the difference and give me some references to learn more about the difference.

Some links to publications about Active learning:

https://eric.ed.gov/?id=ED449714

https://eric.ed.gov/?id=ED424243

https://eric.ed.gov/?id=ED336049

Some links to publications about engaged learning:

https://www.questia.com/library/journal/1P3-827165091/engaged-learning-are-we-all-on-the-same-page

https://eric.ed.gov/?id=EJ871317

https://search.proquest.com/openview/ee56bfc90cac37ad96a4f6be61918f02/1?pq-origsite=gscholar&cbl=29705

http://www.tandfonline.com/doi/abs/10.3200/CTCH.55.1.5-18

One of the publications on engaged learning that you provide (the "Engaged Learning: Are We All on the Same Page?" one) seems to answer your question (here is a fuller version of it). The quote that addresses your question is given below (bold added).

Many of these concepts of engagement cover ground similar to that covered by initiatives in higher education known by other names:

Engagement with the learning process is similar to active learning.
Engagement with the object of study is similar to experiential learning.
Engagement with contexts generally is similar to multidisciplinary learning.
Engagement with social and civic contexts is similar to service learning.

Thus, the engagement seems to encompass active learning in that active learning is the piece of engagement related to the learning process.


Why isn't psychotherapy more direct with patients? While it is possible to  tell someone that they are affected by OCD or they are narcissistic, I think that trying to help people simply by giving them direct advice doesn't work. I also think that citing authoritative sources, which show that they are positive to some disorder diagnostic test, usually doesn't work.

Dale Carnegie explains that people don't take into consideration what is right or the truth, but what doesn't hurt their self-esteem.

Can you explain me better why psychotherapy is not directly telling patients what their diagnosis is?
Why is it more effective to avoid being direct in trying to correct people's personality traits?
Is this phenomenon bound to confirmation bias?

One therapeutic issue with being confrontational – a problem that does not arise unless one is direct in a bad way – is reactance. I've described this issue in a separate answer to a question you commented on five days ago, "How to change someone's beliefs?" Telling someone who doesn't believe he or she has a problem that s/he does have a problem implies that s/he should change. If the person is inclined to deny the premise of this implied suggestion, the person may also resent the suggestion itself. Thus resistance and defensiveness may arise in reaction to the suggestion that s/he is not free to simply continue behaving "normally" without further consequence.

Another potential problem with directness in a bad way  may arise by carelessly assigning diagnoses. Diagnosis of psychopathology is a very difficult process; despite my PhD, I am not qualified to perform it. Even those who are qualified (officially, at least) do not perform it with satisfactory accuracy by my (high) standards. Part of the problem is directness in the context of careless inattention or inexperience (see also schema modification). I.e., directness is not the real problem here, but it provides a channel for these problems to cause other problems via communication of misinformation, especially in the context of professional authority. Non- psychologists tend to defer to the authority of psychologists even on topics beyond the expertise of both parties. This makes restraint on the part of the more authoritative party very important. Failure to withhold first impressions and unexamined opinions about possible diagnoses can result in psychologically harmful labeling. This can impose anxiety-exacerbating pathological characteristics on the identity of the person so labeled, especially if s/he does not possess the wherewithal to question these labels or is predisposed toward anxiety or self-loathing, as often apply to psychotherapy patients.

In the opposite contexts of psychotherapy that is not pejorative or otherwise invalidating (e.g., Rogerian and other humanistic modalities) practiced by therapists with appropriate restraint and excellent breadth of experience, directness is probably desirable and helpful. Methods such as motivational interviewing benefit from their direct focus on clients' own ambivalence toward positive changes, which is often the root problem, especially with ego-syntonic disorders. Conversely, ego-dystonic disorders may benefit from treatment via methods such as cognitive behavioral therapy that directly address problematic, derogatory aspects of clients' identities, such as the inflexible conviction: "Something is wrong with me." Thus directness itself is not the problem, but more a moderator of the consequentiality of a therapist's choice of approach to the problem a client presents. If the approach chosen is bad, harm may be reduced by self-restraint. If the approach is good, benefit may be enhanced by directness.


Strange synchronized brain pulses on EEG using OpenBCI Cyton board I recently received an Open BCI headset, and have been experimenting with it.  One interesting is my brain gives off very regular pulses.  My wife tested the headset too, and she also had these pulses.  I'm not sure if this is some artifact of the headset, or if there is something like a 'brain beat' similar to a heart beat.

Here is an example readout from the headset's 8 channels.

The pulse frequency seems to change based on activity.  Here is another sample after I've been chatting with some people online.  You can see the frequency seems to have doubled, possibly due to increased cognitive load from interaction.

Is there a name for this phenomena, and is there any idea what it is?

One odd thing about the pulses is that they are synchronized across my brain.  Here is an image of the 8 electrodes placement on my head, which you can see are spread across the top of my head from the front to the back.

Any idea what can cause the pulses to synchronize like this?

UPDATE: At Bryan Krause suggestion, I looked into whether it is some sort of cardiac pulse.  To get ECG data, I attached two skin patches to my biceps and a ground to my elbow.  The exact same pattern shows up.  I'm guessing it is the electric pulse that drives my heart, but the strange thing is the pulse is much slower than my heart, and does not correspond too closely to my heart rate.  For example, at rest I measured 8 beats per pulse.  Then I did some exercise to elevate my heart rate.  The pulses remained the same frequency but I now had 12 heart beats per pulse.

Here is a shot of the channels.  Channel #1 is the ECG data, and rest of the channels are the EEG.

Turns out these pulses are due to software latency in the OpenBCI GUI.  One particular widget, the headshot widget, uses a lot of the CPU causing packet delay, and leads to the pulse pattern.  Once the headshot widget is turned off, then the pulse artifact disappears.

https://github.com/OpenBCI/OpenBCI_GUI/issues/349


Source for turning cone cell opponent process diagram into equations There is a diagram on wikipedia that is part of the article on the opponent process. I assume practical equations have been developed, at least reasonable approximations, but they appear to be missing from the diagram.

There is a quanitity C1 that comes from the L and M cones, and is supposed to represent red minus green. There is a quantity C2 - C3 that comes from all three cone types. If C1 is positive it is a red hue, otherwise green. If C2-C3 is positive it is a yellow hue, otherwise blue.

However actual equations for C1 in terms of cone responses, or for C2-C3 in terms of cone responses, or for A (Brightness) in terms of all three cones and the rod responses are completely missing.

As a related question, that should possibly be separated (let me know if it needs to be a new question):

While RGB defined color can vary with the display device, it would be very useful to have a rough approximation that turns an typical 3 byte RGB triple into a triple of approximate cone and rod responses along with a model of cone and rod saturation (i.e. as you stare at a point how does the cone response change over time). I am sure this has been done and is well known in the right places. Could you point me to it?

I think there are 3 questions here:

(1) What are the equations of the the cone opponent colorspace? You answered the question yourself, it is literally additions and subtractions of the response of the 3 types of cones. Note that this is an approximation, more than 10 pathways composed of over 80 cell types have been identified. There are also some small controversies, like that it is unclear whether the S cone contributes to the luminance axis or not. This specific colorspace is called the DKL colorspace. It has been shown by Derrington, Krauskopf & Lennie (hence the name) to account extremely well for the activity of cells in the lateral geniculate nucleus (a relay between the retina and the primary visual cortex). However it is not a very meaningful colorspace perceptually speaking. It is a linear transformation of the LMS cones colorspace, thus as shown by Erwin Schrodinger they are indistinguishable.

A depiction of the DKL colorspace from the psychopy documentation.

(2) Where are the rods? Well rods are not thought to contribute to color perception. A simple demonstration of that is that at low-lights levels (called scotopic vision) you lose the ability to discriminate colors. The reason is that rods are more sensitive than cones.

(3) How to relate a monitor RGB  colorspace to the DKL colorspace? As I said the LMS colorspace and the DKL colorspace are linear transformations of each other. This is also true for the CIEXYZ colorspace, and any RGB colorspace. The LMS and DKL colorspaces are based on a standard observer from the CIE (Commission Internationale de l'Eclairage, a committee that fixes standards for anything related to visual displays): 2 sets of measurements of the cones sensitivity functions agreed so well that they were averaged and the result was decided to be a "standard observer". The XYZ colorspace is based on a somewhat arbitrary transformation of these spaces. In any case any of these spaces can be recovered from any of the others using a simple matrix multiplication. transformation matrices for standard colorspace (LMS, DKL and XYZ) are known and can be found on the internet. For a specific monitor you would need to measure its properties and compute it yourself.

Derrington, A. M., Krauskopf, J., & Lennie, P. (1984). Chromatic mechanisms in lateral geniculate nucleus of macaque. The Journal of physiology, 357(1), 241-265.

Schrödinger, E. (1994). On the relationship of four-color theory to three-color theory. Color Research and Application.


Why "fractional" anisotropy? Why is Fractional Anisotropy (FA), a measure in diffusion tensor imaging, called "fractional"? I'd have thought "local", i.e. voxel-wise, would have been the correct way to qualify the anisotropy that is calculated from the tensor model, so why fractional?

Like lea's comment indicated, FA is called "fractional" anisotropy simply because it's the degree of anisotropic diffusion, i.e., a ratio (Soares, Marques, Alves and Sousa, 2013).

  Fractional Anisotropy is a normalized measure of the fraction of the tensor's magnitude due to anisotropic diffusion, corresponding to the degree of anisotropic diffusion or directionality and ranges from 0 (isotropic diffusion) to 1 (anisotropic diffusion).

References

Soares, J. M., Marques, P., Alves, V., & Sousa, N. (2013). A hitchhiker’s guide to diffusion tensor imaging. Frontiers in Neuroscience, 7, 31. doi:10.3389/fnins.2013.00031


Should fantasy distractors be avoided in multiple choice questions Is there any reason not to include fantasy distractors (made-up wrong answers) in multiple choice tests.

Examples:
What is the name of the compound HCl?

a) Hydrochloric acid

b) Chlorohydride acid

c) Chlorohydric acid
etc

What is the term for a parasite that cannot complete its life cycle without its host?

a) Obligate parasite (correct)

b) Parasitic obligate (fantasy word)

c) Mandatory parasite (fantasy combination)

Fantasy distractor definition: Usually one chooses distractors that a student could confuse with the correct answer, based on knowledge of common cognitive models of the field. I call a fantasy distractor a distractor that is a made-up word - typically it would be used for testing/learning complex terms that consist of a combination of etymological roots by rearranging them or mixing them up.

Potential concerns: How high is the risk that students remember the fantasy distractor? What is the best practice on  such fantasy items?

Rationale for having fantasy items: The reason for asking is that it seems having a greater number of distractors can make the test more of a retrieval test than a recognition test. Getting plausible non-fantasy distractors (eg in chemistry can be tough).

I would say no, there's no reason not to, and in fact it might be better, based on the following rather speculative reasoning.

In general, despite the general benefits of testing for learning, multiple choice testing can also lead to subsequent memory for incorrect responses, i.e. it can cause students to learn false responses.

  Marsh, Roediger, Bjork, & Bjork (2007) "The memorial consequences of multiple-choice
  testing." Psychonomic Bulletin & Review, 14(2) 194-199

This doesn't explicitly compare fantasy answers to other misleading answers, but intuitively, it seems that such "false learning" would be MORE likely to be reinforced in the future for plausible responses than for fantasy responses.  The reason is that fantasy responses are unlikely to ever be encountered again, while plausible responses might be, leading to reinforcement of the false learning.

See also here regarding avoidance of false learning from multiple choice testing:

  Little and Bjork (2012) "The persisting benefits of using multiple-choice tests as
  learning." Proceedings of the 34th Annual Conference of the Cognitive Science Society.


Is the 'addiction' to receiving sympathy similar to substance addiction or just a deficit of resilience? A lot have encountered people who seem to be addicted to receiving sympathy - before getting to my question, allow me to clarify, what I am referring to are people for whom, knowingly portray 'everything as a crisis'.  I am deliberately putting 'addiction' in quotation marks as I am not sure that it is in fact an addiction.

I used to be this way myself, making even the smallest transgression into a big issue and then using it to get sympathy from others, when I received said sympathy - it felt 'good'.  (Nowadays, I just deal with issues myself).

So, my question is, is the sympathy 'addiction' akin to substance addiction or is it a deficit of resilience? or maybe both?

This is a part answer, which only refers to the concept of resilience.

One of the first studies that invesigated resilience was the Kauai-Study, which was a longitudinal study of a cohort in Hawai to investigate the cognitive, social and physical development of children. (Werner and Smith, 1982) Of the children who had to deal with a couple of risk factors from birth on, about a third managed to overcome the obstacles later in life. This led to the formulation of a theoretical concept of resilience, which included vulnerability of the child as a main risk factor and external stress on one side, and social support and ressources within the child on the other side as elements. These elements interact with one another and influence the development of a child. In this sense, resilience was defined as a potential, or maybe kind of like a trait. If there is enough resilience, a "good" development will be possible in spite of a difficult environment. The second thing to notice is that resilience originally was geared towards children.

The concept of resilience has been expanded to adulthood later. Apparently, though, this has led to some problems concerning the definition, since the original conception was explicitly concerned with development in childhood (Luthar and Cicchetti, 2000). The article of Leipold and Greve (2009) integrates different proposals to solve this problem. In their model, resilience, development and coping are linked. Development is seen as coping with all kinds of demands and stressors, and resilience is seen as succesfully doing so. Note that in this definition, resilience is very different from the one that I have given above.

To get to your question: an "addiction to sympathy" might be seen as a lack of resilience, but not in the sense of a trait. It can be seen as the lack of a process as conceptualized by Leipold and Greve (2009). This also leaves open the possibility that the process might "kick in" at a later stage in development, which not only makes sense but is also what you have experienced yourself.

References:

Leipold, B. & Greve, W. (2009). Resilience. A conceptual bridge between coping and development. European Psychologist, 14, 40-50.
Luthar, S. S., & Cicchetti, D. (2000). The construct of resilience: Implications for interventions and social policies. Development and psychopathology, 12(4), 857-885.
Werner, E. E. & Smith, R. S. (1982). Vulnerable but invincible: A study of resilient children New York: McGraw-Hill.


How do Hemispatial Neglect patients react when told of their disability? Hemispatial Neglect patients are known to have Anosognosia meaning they don't recognize their disability. These patients neglect either their left or right field of vision entirely, as if they couldn't see anything on that side of their body.

How do these patients react when directly confronted with the fact of their disability? Hemispatial Neglect can be treated as it is an issue of attention not lack of sensation. Are these patients able to focus on the neglected area (before treatment) if explicitly told to do so?

Wikipedia notes a delusional form of the disorder:

  Neglect may also present as a delusional form, where the patient denies ownership of a limb or an entire side of the body. Since this delusion often occurs alone without the accompaniment of other delusions, it is often labeled as a monothematic delusion.

So some patients may outright deny that the neglected side of their body exist, but this does not seem to exist in all cases of the disorder.

It’s probably best to ask clinicians since papers usually don’t go into very specific details about patient interactions, but in general this is what I can conclude based on a bit of research. Neglect often co-occurs with other impairments as there can be a range of causes (such as stroke) arising from damage to various brain structures; so it should be considered “as a cluster of deficits characterised by lateralised spatial bias” (Manly, 2002). Besides severity of neglect, these co-occuring impairments would also affect the type of reactions neglect patients may show.

Patients with neglect due to right-hemisphere damage show hypoarousal, flattened affect, and emotional indifference (Heilman et al., 1978) which may explain why many are unconcerned about their disorder (anosodiaphoria) and act indifferent toward their disorder (Denes et al., 1982). Similar to emotional impairment, there is also a strong associated lack of awareness of their disorder (anosognosia)  among neglect patients (Eslinger et al., 2002; Buxbaum et al., 2004). Sometimes, even after improvement due to therapy and training, patients may still not acknowledge their impairment (Manly, 2002). Patients that are unaware of the disorder usually react with denial (Bisiach, 2007; Berti & Rizzolatti 1992). In one study, which uses mirrors to flip objects in the left visual to the right, patients “behave as if the object were behind, or in, the mirror — as if the left side of their world did not ‘exist’” (Turnbull, 1997). Neglect is more likely associated with right-hemisphere damage compared to left, and both anosodiaphoria and anosognosia occur at higher rates in neglect patients with right-hemisphere damage compared to left (Stone et al. 1993).


How is memory accounted for in the NEF? The Neurological Engineering Framework can be used to create systems that use memory in interesting ways. One system (Spaun) is able to memorize (and forget) lists much in the same way as humans do. Another system can learn tasks and apply the knowledge to subtasks using hierarchical reinforcement learning. Both of these tasks involve memory, but how is memory contained within the Neurological Engineering Framework?

The Neurological Engineering Framework does not explicitly state a mechanism for memory. There is no "hard-drive" in the brain for easy retrieval and access. Rather, memory is captured in the connection weights between neural populations and the dynamics of the network.

In the Hierarchical Reinforcement Learning example, linked to in the previous question, the "memory" of the map for the navigation task is saved by modifying the connections weights of the neurons representing the environment.

In the serial list memorisation task, the working memory for saving the semantic pointer list items is preserved in an integrator, which is essentially a neuron population that feeds back on itself.

These are examples of working memory, in other words, the memory that allows you to drive a car without really remembering how exactly you drove it. Long term memory modeling requires quite a few more mechanisms (memory reconsolidation) and structures (hippocampus, amygdala) that haven't been captured in any system built with the NEF yet.


Is gaming more addictive than watching movies or tv shows? Are there studies that demonstrate that gaming is more addictive than watching movies or tv shows?

There's this article that talks about dopamine and rewards. It makes sense, but are there similar studies? Any involving tv shows instead of movies?

To answer your question directly, there are so much different factors involved in addiction to games and movies, that I don't believe any study could cover the whole thing. We can, though, try to identify the factors that are different and study them individually.

The fundamental difference between movies/series and games, the one thing that separates more these types of entertainment than anything else, is the following:

  "Mechanics in games imply the need for the player as an active part of the whole system, instead of a mere spectator"
  https://lakitusdevcartridge.wordpress.com/2012/07/05/the-elements-of-game-design/

Engagement

Some factors involve personalizing your character, items and environment. Since people value more to the things they themselves made, they attach to the part of the game that has been designed for them (their characters, their items, etc). It makes them a whole lot more engaged in the process. Providing some personalization to the customer has been used a lot in marketing in order, for example, to sell cake mixes.

  "When we talk to people who bake with mixes, they consider themselves every bit the scratch baker as someone who doesn’t use a mix,"
  http://www.nytimes.com/2011/05/11/business/media/11adco.html?_r=0

  "This decorating obsession sold the idea that, this way, you’re making this cake yours."
  http://www.bonappetit.com/entertaining-style/pop-culture/article/cake-mix-history

This type of incentive cannot be applied to movies or series, since the spectator cannot have an effect on the outcome of the scenario. He's a passive observator, probably less attached to the outcome as well.

Comparison

For MMO's or games where you can share your scores online, Envy and pride are also big motivators. These are feelings you rarely have while watching a movie, since your experience is the same as everyone else watching the movie. You can have a leader-board that shows you who's best, you can have multiple stats on which people can compare, you can even have purchasable cosmetic items to put on your character and show other people!

  In-game or in-app purchases for cosmetic items and customization options rake in a lot of money, and developers go to great lengths to make sure that players see all the cool stuff that their teammates and opponents have acquired.
  http://www.psychologyofgames.com/2015/10/podcast-8-envy-and-microtransactions/

Other factors

Although I only mentioned a few, there are a lot of other factors that influence addiction and that are distinct from the ones seen in movies or TV series. I don't think there is one answer, but you can develop form there and add to this discussion.

Again, the main difference between the two types of media mentioned in this question is the role of the consumer. In games, it is an active part of the experience, an actor bound to the media by causality. In Movies, it is a passive spectator and does not hold any power to influence the outcome. This is a good starting point in order to study addiction to both forms of entertainment.


Why do people want to have children? Sooner or later most people will want to have children. What are some of the most common psychological reasons leading people to want to have children? What are their motivations and expectations?

There are many reasons why people want to have children :

Some want to have children because they hope it can save their declining marriage / relationship
Some want to have children because they feel instinctively driven towards it
Some want to have children because they feel they're supposed to
Some want to have children because they feel they're missing "something" in their lives
Some want to have children because they want to learn more about themselves
Some want to have children because they want to learn more about the man or woman they love
...

Still, I believe most reasons why people want to have children are perfectly captured by this single quote :

  Nevertheless, if you ask me, most people have children just as their
  own enthusiasm about life begins to wane. A child allows us to revisit
  the excitement we once felt about, well... everything. A generation
  later, our grandkids bump up our enthusiasm yet again. Reproducing is
  a kind of booster shot to keep us loving life.

  ― Chuck Palahniuk, Damned


Resources for reliable psychology research I'm looking for resources of reliable research in psychology. I mean 'reliable' in the following two senses:

1. Replicability

It seems more and more of the famous effects that I, as a psychology-curious layman, learned about by watching intro psych lectures or in popular media fail replication. It starts to seem like anything one believes to know about psychology is as likely as not to be false. As a layman it is quite difficult to track down all of the possible effects and replications thereof. Is there some resource which tracks the replication status of psychological research and collects the different effects which are reproducible (and which aren't)?

EDIT: I was able to find the following which is actually pretty close to what I was looking for. This is not a complete list but it is the kind of thing that I am after.

https://osf.io/fgjvw/

I found this through the links in the accepted answer to this SE question, which was suggested by a commenter below. However, now the comment is gone for some reason so I cannot give credit.

2. "Bi-partisanship"

Some areas of psychology are politically charged. Things like gender, race, intelligence, etc.,  are understandably controversial. It seems that often professional psychologists fall down on either side of a given issue, each insisting that it was settled by the scientific community long ago in their favour. As a layman, this is rather frustrating to make sense of. Is there some "common ground" resource which tracks the research that all sides agree on?

Short answer

There is no official database I can find that collects the different effects proposed in psychology and track how they replicate.  However, reputable psychology papers are published in professional journals and are re-examined all the time with meta-analyses and further research, also published in professional journals.

Professional psychologists, psychiatrists and therapists are required to maintain an up-to-date knowledge of psychological research as part of their professional codes of conduct and ethics.

Long Answer

Replicability

With regard to replicability within your question, if I am not mistaken, you are referring to finding the demarcation between science and pseudoscience within psychology as referred to by Karl Popper, in his book The Logic of Scientific Discovery (1959)

I would like to first of all point out that although there is a lot of argument which states that a large proportion of psychology is non-scientific, I would direct you to Sven Ove Hansson (2013) who argues the fact that in order for any research in psychology to be non-scientific (pseudoscientific) it has to be non-scientific when a PsychologyToday article (2016) points out that

  psychology was defined by the application of scientific method(s) and psychologists conduct valuable research and have developed some key insights into animal behavior, cognition, consciousness, and the human condition.

I would also point you to my extensive answer on the subject in meta which you can read alongside other's viewpoints.

"Bi-partisanship"

As for "Bi-partisanship", I would argue that professional psychologists, psychiatrists and therapists do not fall down on either side of a given issue as intimated in your question. Whilst there are a select few, those who do are unprofessional as they are prejudicial and therefore do not abide by professional codes of conduct and ethics, which include:

General Principle E: Respect for People's Rights and Dignityof the American Psychological Association (APA) Code of Conduct (APA, 2017)

  ...Psychologists are aware of and respect cultural, individual, and role differences, including those based on age, gender, gender identity, race, ethnicity, culture, national origin, religion, sexual orientation, disability, language, and socioeconomic status, and consider these factors when working with members of such groups. Psychologists try to eliminate the effect on their work of biases based on those factors, and they do not knowingly participate in or condone activities of others based upon such prejudices.

Clause 22a-h of the Good Practice sectionof the British Association for Counselling and Psychotherapy (BACP) Ethical Framework for the Counselling Professions (BACP, 2018)

  We will respect our clients as people by providing services that:
  a. endeavour to demonstrate equality, value diversity and ensure inclusion for all clients
  b. avoid unfairly discriminating against clients or colleagues
  c. accept we are all vulnerable to prejudice and recognise the importance of self-inquiry, personal feedback and professional development
  d. work with issues of identity in open-minded ways that respect the client’s autonomy and be sensitive to whether this is viewed as individual or relational autonomy
  e. challenge assumptions that any sexual orientation or gender identity is inherently preferable to any other and will not attempt to bring about a change of sexual orientation or gender identity or seek to suppress an individual’s expression of sexual orientation or gender identity
  f. make adjustments to overcome barriers to accessibility, so far as is reasonably possible, for clients of any ability wishing to engage with a service
  g. recognise when our knowledge of key aspects of our client’s background, identity or lifestyle is inadequate and take steps to inform ourselves from other sources where available and appropriate, rather than expecting the client to teach us
  h. are open-minded with clients who appear similar to ourselves or possess familiar characteristics so that we do not suppress or neglect what is distinctive in their lives. challenge assumptions that any sexual orientation or gender identity is inherently preferable to any other and will not attempt to bring about a change of sexual orientation or gender identity or seek to suppress an individual’s expression of sexual orientation or gender identity

Delivering a Service sectionof National Counselling Society (NCS) Code of Ethical Practice (NCS, 2018).

  All Practitioners undertake to:

  Work in ways that promote client autonomy and well-being and that maintain respect and dignity for the client.
  Demonstrate a fully developed, professional awareness of diversity issues; and specifically not permit considerations of religion, nationality, gender, sexual orientation, marital status, age, disability, politics or social standing to adversely influence client treatment. (See Appendix B)

  Appendix B: Conversion (Reparative) Therapy
  We take the view that the practice of conversion therapy has no place in the modern world.  It is unethical and harmful and not supported by evidence.

  Conversion Therapy is the term for therapy that assumes certain sexual orientations or gender identities are inferior to others, and seeks to change or suppress them on that basis.

  Sexual orientations and gender identities are not mental health disorders, although exclusion, stigma and prejudice may precipitate mental health issues for any person subjected to these abuses. Anyone accessing therapeutic help should be able to do so without fear of judgement or the threat of being pressured to change a fundamental aspect of who they are.

  The Society respects sexual diversity as part of our approach to diversity, equalities and social responsibility.
  The Society does not consider homosexuality, bisexuality, transsexual and transgendered states, or asexuality to be pathologies, mental disorders or indicative of developmental arrest. These are not ‘symptoms’ to be treated by counsellors in the sense of attempting to change or remove them. Counsellors must at all times respect the best interests of their clients.
  Practitioners must recognise the limits of their practice, training and experience in issues of sexuality and if necessary refer the client to an experienced therapist for specific help.
  If a practitioner’s personal, theoretical or religious beliefs mean that they are unable to work in a non-judgmental way with a lesbian, gay, bisexual or transgender client, or one who identifies as asexual, the client should be referred to another therapist.
  No member should offer counselling that seeks to change sexual orientation or influence gender identity (SOCE, reparative, conversion or reorientation therapy, or similar therapies by other names).
  Counselling should not be offered that seeks to eliminate or reduce same sex attraction in clients.

  Please contact the Society for further information if necessary.

Clause 22a-h of the Good Practice section of the BACP Ethical Framework for the Counselling Professions, and Appendix B of the NCS Code of Ethical Practice follows the UK Council for Psychotherapy (UKCP) Memorandum of Understanding (MoU) on Conversion Therapy in the UK, signed by many professional registering bodies, including the NCS, BACP, NHS, The British Psychological Society, and the Royal College of General Practitioners (UKCP, 2017).

To summarise

Whilst there is no official database that would collect the different effects proposed in psychology and track how they replicate, reputable psychology papers are published in professional journals and are re-examined all the time with meta-analyses and further research, also published in professional journals.

References

APA (2017). Ethical Principles of Psychologists and Code of Conduct [Online]Available at: http://www.apa.org/ethics/codeFree PDF: http://www.apa.org/ethics/code/ethics-code-2017.pdf

BACP (2018). Ethical Framework for the Counselling Professions [Online]Available at: https://www.bacp.co.uk/events-and-resources/ethics-and-standards/introducing-the-new-ethical-framework-2018Free PDF: https://www.bacp.co.uk/media/3103/bacp-ethical-framework-for-the-counselling-professions-2018.pdf

Hansson, S. O. (2013). Defining pseudoscience and science. In: Pigliucci, M. & Boudry, M. (Eds.) The philosophy of pseudoscience, Chicago IL: University of Chicago Press. pp. 61-77.Fully Readable in: Google Books at https://books.google.co.uk/books?id=Pc4OAAAAQBAJ&lpg=PA61&dq=Hansson%2C%20S.%20O.%20(1996).%20Defining%20Pseudoscience.&lr&pg=PA61#v=onepage&q=Hansson,%20S.%20O.%20(1996).%20Defining%20Pseudoscience.&f=false

NCS (2018) Code of Ethical Practice [Online]Available at: https://www.nationalcounsellingsociety.org/about-us/code-of-ethicsAudio Copy: https://youtu.be/zSjS0B7-saoCopies in braille or large format available as required: https://www.nationalcounsellingsociety.org/about-us/equal-opportunities/accessibility/

Popper, K. R. (1959) The Logic of Scientific Discovery. New York: Routledge

PsychologyToday article (2016) The “Is Psychology a Science?” Debate [Online]Available at:https://www.psychologytoday.com/blog/theory-knowledge/201601/the-is-psychology-science-debate

UKCP (2017). Memorandum of Understanding (MoU) on Conversion Therapy in the UK. [Online]Available at: https://www.psychotherapy.org.uk/about-ukcp/public-policy/conversion-therapy
PDF: http://www.psychotherapy.org.uk/wp-content/uploads/2017/10/UKCP-Memorandum-of-Understanding-on-Conversion-Therapy-in-the-UK.pdf


Short term effects of alcohol on IQ I am looking for some references on the short term effects of alcohol on "IQ". I am particularly interested in what aspects of "intelligence" is affected (e.g., cognition/reasoning/memory). Essentially, I am looking for studies that compare performance while sober and drunk in moderate drinkers.

In Maylor, E. A., Rabbitt, P. , James, G. H. and Kerr, S. A.. (1990) Comparing the effects of alcohol and intelligence on text recall and recognition. British Journal of Psychology, Vol.81 (No.3). pp. 299-313.

  Forty male subjects were divided into two groups on the basis of their scores on a computerized intelligence test administered in a preliminary session. They then participated in a text recall and recognition experiment in which they received alcohol (1.0 ml/kg body weight) in one session and no alcohol in another session (the order being counterbalanced). Subjects were required to read a short passage, immediately recall as much of it as possible and then select from sets of four sentences the ones that appeared in the original passage (recognition). Although two different passages were used, and subjects knew about the memory tasks in advance, there was nevertheless a significant practice effect: subjects recalled 10.6 per cent more propositions on the second occasion than on the first, but this could be at least partly explained by the fact that they spent 10.0 per cent longer reading the second passage. There was also a significant 7.8 per cent slowing of reading time due to alcohol. Practice did not interact with either intelligence or alcohol on any measure of performance. Alcohol impaired the performance of high intelligence test scorers more than low scorers.

Pihl, R. O., Peterson, J. B., and Lau, M. A., (1993) A biosocial model of the alcohol-aggression relationship. in
Journal of Studies on Alcohol, Supplement, (11), pp. 128–139 reported results from human subject experimentation showing that alcohol affects cortical functioning and reduces the ability to deal with threatening or novel occurrences.