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Dear fellow researchers, I would like to design an experiment related to relationships and bonding, which involves measuring the level of oxytocin in humans. So, could you please share the best way to measure the oxytocin level? Is there any Neuroimaging for measuring hormones level? Thank you very much!
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Here's a nice paper on ways to measure oxytocin levels in humans: https://www.nature.com/articles/s41598-017-17674-7
Unfortunately, it doesn't appear as if you can image oxytocin using MRS (which has pretty poor spatial and temporal resolution anyway) or any other neuroimaging measures as far as I can tell.
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I know that it could be different for each situation, but when I was gathering data from participants in the pilot phase of my study, I've realized that if I explain the instructions aloud it could be more effective than letting them read those. Now my supervisor insists that I refer to a scientific document for this. the experiment was designed with a masking paradigm and the instructions contained content with positive and negative reinforcement.
Does anyone know any reference?
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I think you can safely write that research shows an overall gain with oral presentation for both students with and without disabilities. References you can quote on this are
2)
and especially this meta‐analysis of Research on the read aloud accommodation
Wishing you fun with your research, Mohammad
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I am planning to do an experiment on gamma wave binaural beats of 40 Hz. I have downloaded this video https://www.youtube.com/watch?v=mQXNCwfqRjo from youtube. I was wondering if anybody could help me with the information regarding -
how to make sure about the video of 40 Hz?
and how to find the exact frequency of right and left side of auditory stimuli?
Would really appreciate your help. Thank you.
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I also think the cognitive effects of binaural beats are interesting but the results are mixed so it is good if you are planning to do some study that could perhaps clarify the picture. Yes, both sides should be there if you increase the size parameter in the Plot frequency window. You could separate the stereo channels and do the analysis for each to make sure it is separated. https://manual.audacityteam.org/man/splitting_and_joining_stereo_tracks.html
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Dear colleagues,
Do you have an idea about the source of light through which we see dreams ? and what is the source of light through which we can see the colors we see in dreams?
I wish you all the best
Huda
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Blind people have no visual imagery in their dreams, if born blind. Dreams do process past memories; in a dream, different temporal memory layers can be mixed over into 'one film'. We do not dream with our eyes, it is a brain function in sleep as the brain is a non-stop organ (you could put a light bulb on it).The existence of pre-cognitive dreams, which is portrayed in prophetic literature, e.g. Joseph in Egypt, cannot be ruled out. A healthy sleep cycle (chronobiology) and dreamimg are closely connected, in medical terms, to 'free' the memory from non-necessary psycho-logical ballast of life experiences.
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I intend to carry out Spatial Navigation evaluations in the elderly with low level of education.
Thank you!
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To my knowledge, there is no so-called "gold standard" but there are "tried-and-tested" methods. A most popular approach has been the use of virtual environments (designed using game engines like Unreal and Unity) in the testing of older adults in computer labs (see Zhong & Moffat, Zhong,Magnusson, et al., 2016).
Alternatively, you can always resort to the traditional method of testing the spatial orientation ability of your participants in the real world through guided navigation of a previously unfamiliar environment and getting them to perform pointing-to-landmarks and distance estimation tasks (see Zhong, 2013; Zhong, 2016; Zhong & Kozhevnikov, 2016). 
Please refer to all the links below. I pray that you shall find these/my papers useful. You will find other studies of relevance in the reference pages of these papers.
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Researchers from indigenous background 
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KICA - Kimberley Indigenous Cognitive Assessment Tool and Cogstate ( Computer based) are good tools. KICA is mainly for above 45.
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I was attempting to use computerized tasks within my research project, however I have been unable to crack PsyScope (and lack the technical support to do so). I wondered if anyone knew of any visual inhibition and shifting non-computerized tasks. Thank you!
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Try the Inhibition test from the NEPSY-2.  I find it very helpful.
good luck,
ray
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Stimuli consist of dichotic pairs from the set of ba,ga,da,ta,pa,ka.  Subject is instructed  to report stimulus heard most clearly. Data is tabulated as percent correct responses. Does this mean that an incorrect response would be saying TA when the stimulus pair was e.g. BA,GA. If that is so, does anybody correct for guesses?
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I think that the main thing you need to focus on in this test is the number of correct responses from each ear. May be you really have some trials when your subject can give you a correct answer  for guesses. The best thing you can do to clean your data is to exclude from the sample those subjects who had a lot of incorrect answers (for example, more than two standard deviation). 
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We're looking for some norms for older individuals on the digit span task. Although there seem to be a lot of sources that report norms, very few report how accurate the participants were at the various different serial positions. We're especially interested in recency effects, so this information is crucial.
Anyone know of anything?
Thanks
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As Rob alludes to, the digit span task is designed to measure the maximum list length for which recall is accurate / correct. As such, serial position effects are not so meaningful, because by definition performance is at ceiling up to span (ok not completely true but as a first approximation this holds)
You can administer individually-titrated span or supra span list lengths and then you are likely to observe serial position curves, but at this point you are investigating serial recall, not span.
This is not a simple configuration environment for which to produce norms. For example, many researchers would anticipate different levels of serial recall accuracy depending on just how supra-span the list is, they might expect primacy or recency to vary with details such as presentation rate, and if you are using a digit span task, then there are constraints such as the size of the stimulus set (i.e. you only have 9 stimuli to play with, and they therefore repeat across trials). In other words, norms might be so study-specific or of such limited generalisability that they aren't really norms at all.
My expectation is that most studies, like those you cite, use control groups for exactly these reasons: to provide some meaningful reference point for the ageing data of interest.
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We are going to perform three OF behavioral analysis in 1, 6 and 15 month-old Wistar rats. However, we are in doubt as using the same squared area for different sized animals. Is there any gold-standard for OF test troubleshooting, especially regarding area per animal? If there is, does changing the OF size for larger animals still a valid way to prevent area-dependent influences, or must I keep the very same paradigm for all animals?
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I agree that size of the animal (and considering the answers above, also age of the animal, which particularly in rats has a major effect on their size) does have an influence. Within an experiment all animals should be tested in exactly the same conditions, including OF size. If one of your aims is to compare specific behavioral aspect in animals (e.g. rats of a specific strain) of different age (i.e. size) cage size again should not be different. So you see, it all depends on your question and protocol. Time of day of the test and lighting conditions and the adaptation to the animals to them has an often underestimated effect on behavior of rats and mice.
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Hello everyone, i like to ask about behavioral models or trials to apply in rats (preferably Sprague Dawley rat) about the study of time perception, time lapses or similar.
Thanks all of you!
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You can use a temporal discrimination operant task in rats (see link below).  You train the rats so that, for example, if a tone comes on for 2 seconds they press a certain lever for a reward, but if the tone comes on for 8 seconds they press the opposite lever for the reward.  Other operant tasks also have a time perception component to them.  For example, the DRL-72 task requires the rats to wait 72 seconds before pressing the lever for a reward.  You could also adapt this task to change the DRL requirement to different times based on different cues.  The delayed discounting task also has a time perception component to it, as the longer the time for the delayed reward is perceived, the less valued the delayed reward will be to the animal.
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We usually run experiments in which several participants (typically visual LDT) simultaneously do the task. I wonder if this may affect experimental results because of attention or just subtle group interaction may distract or press some participants during performing the task.
Does someone know if this methodological point has been treated in some paper?
Thank you!
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There is a long-standing concept of social facilitation, whereby people (and rats) perform simple tasks better in the presence of others. 
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I wonder if it could be treated as a gold mandibular dystonia sporadic or anxiety disorder.
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'Sorry, my approach is muscular, through relaxation (TREPOKS method), and non-specific in first phases.
But I'm interested by the topic, because is a clinical problem, usually detected by dentists.
Regards,
VhiK.
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At which recording sites should I try to describe such components when I use an average reference?
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Can you tell us a little more about your experiment?  E.g., design, what you're manipulating, what components you are most interested in, etc.? 
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I'm currently doing BDA (biotinylated dextran amine) injections into the motor cortex for anterograde axonal tracing. My BDA is tagged with Alexa 488 and Alexa 564. The biggest issue I'm having at the moment is that my BDA is staining the pia mater of my brain and appears to be going everywhere! I think it's contributing to some of the vessel staining I'm seeing as well. 
I've tried varying speeds and amounts of injected BDA. Pulling the needle out slowly, but none of this seems to be really reducing the spillage. 
I've attached a picture so you can see the staining all along the edge of the brain. 
Has anyone who has done this procedure before encountered this problem?
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Are you pressure injecting or iontophoretically injecting BDA?  If the former, what is the volume you are injecting?  It is possible that there will be tracer leakage out of the penetration and around the skull a little time post-surgery considering you are injecting a cortical, or superficial structure.   I have seen similar cases with 'autofluorescence' of pia mater only when I pressure inject FR and a number of AAVs.
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Damasio et al. propose that somatic markers (feedback signals representing homoeostatic and other bodily states) play a pivotal role in our decision-making processes. The ventromedial prefrontal cortex (VMPFC) is identified as the cerebral module of most relevance to the somatic system. Emotions are understood by SMH advocates as the feeling of the bodily states reported by the markers. Sufferers of damage to the VMPFC have consistently demonstrated anomalous emotional dispositions accompanied by poor decision making (both time-costly and poor outcomes), in the absence of further detrament (no loss of iq, working memory...). The role of emotions in decision making is proposed to be that of restricting the options put up for conscious consideration, based on biasing signals from the body. There is here a suggesting of tacit learning by the body, prior to conscious knowledge. (See the Iowa gambling task)
Smith and Elsworth (1985) and apparently others since then have identified six "cognitive appraisal dimensions" that can help distinguish emotions. Certainty, pleasantness, attentional activity, control, anticipated effort, and responsibility are all features of appraisal patterns underlying distinct emotions, and helping to define them.
Thus, we may find that certain emotions such as happiness and anger may share more relevant features than two emotions of the same valence (positive/negative). Since happiness and anger both construe appraisals of certainty and a sense of individual control over the situation, such cognitive dimensions might play a bigger part in determining the nature of the decisions made than the simple positive/negative valence distinction alone.
Do such considerations necessary undercut the Somatic Marker Hypothesis? Is there room for it to accept such dimensions to our emotions, without selling itself short?
Many thanks
Adam
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Dear Adam, there is no evidence for somatic states directly influencing appraisal. The influence should be by means of brain systems. The problem is that functional anatomical hypotheses as the involvement of ventromedial PFC in appraisal do not distinguish between a brain system that instantiates the somatic feeling and a brain system that makes the cognitive appraisal. This kind of distinction is made in the attached paper that proposes that the neuronal network makes the cognitive job and the astroglial network instantiates feelings.
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What are the advantages of email therapy from the therapist's perspective? From the patient's perspective?
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In some cases it can be a problem because the person who receives it will read the message with the "tone" according to his mood at the moment. He is not feeling well already, what if he reads the message with sarcasm, or as if the therapist were fighting with him? Another aspect of such messages is that people tend to use this message as an unrefutable message. On direct contacts we can question, agree with part of the message and  in written we tend to accept it without any questioning. So, it is a great and strong means of approaching a patient. The therapist has to be exteemely cautious. From far, a therapist does not speak to one's minds, he screams to people's minds and the message will not be printed on paper, but on stones. 
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Do you think (among other things) it measures executive functioning?
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Hey Judy!  Don't you think it measures almost everything, that is why it has emerged as so sensitive to lesions anywhere in the brain? It demands attentional control, attentional switching, graphomotor control, associative learning, visuospatial processing, kinesthetic processing, and executive control/cognitive control...
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The following is a recurrent issue in our study and by now no consensus have been reached in my team. 

We made our subjects to perform some neuropsychological tests. An italian validation sample is availlable for all of them and their manuals provide instructions to correct the raw scores accordingly (stratified by: age, gender, and schooling).
In our studies, we inserted the corrected scores in a regression model as independent variables, but we decided not to insert also age, gender and schooling as covariates. Considering the previous correction process, we thought that the confounding effect of these variables has already been controlled for and there is no need to do it in the regression model. Inserting age, gender and schooling would result in no further correction (at the expense of an increase in the number of predictors) or even in a possible "overcorrection" in some situations.
However, some others point doubts on this, saying that the insertion of the covariates in the model is anyhow necessary.
What do you think is the most correct procedure?
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Y
Yes it is a good point. So, I guess that it is important to observe the correlation matrix too check the dependence between variables, the neuropsychological tests and explanatory variables. Anyway, If you have some doubt you can put together in a stepwise process for check this collinearity.
I am really fan to do statistics with strong background in ideas more than by "numeric way", if you believe that to variables and the variable are independent it is better to do the statistics without it. If you are not sure it is better to check this kind of effects, it is possible that two variables are independent but when the variable appears become dependent. If you don't check it you can to have problems with the referee.
Of you now how to use R software you can run this code. And you understand that I mean. I put the results of R console, hence you can check the results (even if the program is not familiar for you)
Good luck and better research. Cheers
#################################################################
set.seed(10) # Fix seed for the random varibles
# Create variables
x1 <- rnorm(n = 100, mean = 100, sd = 5)
x2 <- rnorm(n = 100, mean = 1, sd = 0.5)
Error <- rnorm(n = 100, mean = 0, sd = 1)
y <- 2* x1 + x2 + 1 + Error
# Model with stepwise
mod <- Rcmdr::stepwise( lm(formula = y ~ x1 + x2))
summary(mod)
BIC(mod)
# Other models
summary(lm( y ~ x1))
BIC(lm( y ~ x1))
# X2 it is idenpendet
summary(lm( y ~ x2))
BIC(lm( y ~ x2))
# Correlation matrix
cor(cbind(y, x1, x2))
# Results
# > set.seed(10) # Fix seed for the random varibles
#
# > # Create variables
# > x1 <- rnorm(n = 100, mean = 100, sd = 5)
#
# > x2 <- rnorm(n = 100, mean = 1, sd = 0.5)
#
# > Error <- rnorm(n = 100, mean = 0, sd = 1)
#
# > y <- 2* x1 + x2 + 1 + Error
#
# > # Model with stepwise
# > mod <- Rcmdr::stepwise( lm(formula = y ~ x1 + x2))
#
# Direction: backward/forward forward/backward backward forward
# Criterion: BIC
#
# Start: AIC=5.47
# y ~ x1 + x2
#
# Df Sum of Sq RSS AIC
# <none> 92.0 5.47
# - x2 1 12.3 104.3 13.44
# - x1 1 8740.5 8832.5 457.31
#
# > summary(mod)
#
# Call:
# lm(formula = y ~ x1 + x2)
#
# Residuals:
# Min 1Q Median 3Q Max
# -2.65155 -0.56638 0.07495 0.65964 2.35925
#
# Coefficients:
# Estimate Std. Error t value Pr(>|t|)
# (Intercept) 1.29398 2.09137 0.619 0.537547
# x1 1.99993 0.02083 96.000 < 2e-16 ***
# x2 0.72901 0.20226 3.604 0.000496 ***
# ---
# Signif. codes: 0 ‘***’ 0.001 ‘**’ 0.01 ‘*’ 0.05 ‘.’ 0.1 ‘ ’ 1
#
# Residual standard error: 0.9739 on 97 degrees of freedom
# Multiple R-squared: 0.9896, Adjusted R-squared: 0.9894
# F-statistic: 4610 on 2 and 97 DF, p-value: < 2.2e-16
#
#
# > BIC(mod)
# [1] 293.8658
#
# > # Other models
# > summary(lm( y ~ x1))
#
# Call:
# lm(formula = y ~ x1)
#
# Residuals:
# Min 1Q Median 3Q Max
# -3.1596 -0.6223 0.1859 0.7493 2.6301
#
# Coefficients:
# Estimate Std. Error t value Pr(>|t|)
# (Intercept) 2.42117 2.19071 1.105 0.272
# x1 1.99557 0.02203 90.571 <2e-16 ***
# ---
# Signif. codes: 0 ‘***’ 0.001 ‘**’ 0.01 ‘*’ 0.05 ‘.’ 0.1 ‘ ’ 1
#
# Residual standard error: 1.032 on 98 degrees of freedom
# Multiple R-squared: 0.9882, Adjusted R-squared: 0.9881
# F-statistic: 8203 on 1 and 98 DF, p-value: < 2.2e-16
#
#
# > BIC(lm( y ~ x1))
# [1] 301.8295
#
# > # X2 it is idenpendet
# > summary(lm( y ~ x2))
#
# Call:
# lm(formula = y ~ x2)
#
# Residuals:
# Min 1Q Median 3Q Max
# -20.9307 -6.9010 -0.0086 6.8308 23.5475
#
# Coefficients:
# Estimate Std. Error t value Pr(>|t|)
# (Intercept) 200.9947 2.1016 95.641 <2e-16 ***
# x2 -0.3978 1.9684 -0.202 0.84
# ---
# Signif. codes: 0 ‘***’ 0.001 ‘**’ 0.01 ‘*’ 0.05 ‘.’ 0.1 ‘ ’ 1
#
# Residual standard error: 9.494 on 98 degrees of freedom
# Multiple R-squared: 0.0004167, Adjusted R-squared: -0.009783
# F-statistic: 0.04085 on 1 and 98 DF, p-value: 0.8402
#
#
# > BIC(lm( y ~ x2))
# [1] 745.7054
#
# > # Correlation matrix
# > cor(cbind(y, x1, x2))
# y x1 x2
# y 1.00000000 0.99407964 -0.02041253
# x1 0.99407964 1.00000000 -0.05803451
# x2 -0.02041253 -0.05803451 1.00000000
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GSR has been used to determine stress levels, cognitive dilemma and response inhibition during tasks. My subjects completed brief surveys and a belief questionnaire while skin conductance levels were collected every .05 seconds. With my software, I am only given the GSR levels and timing as well as a simple visual line graph.
I would like to know how to measure overall fluctuation during the task. While the graph shows me "significant differences". Averages and standard deviations are "insignificant." I'm assuming there is a definite way to measure overall fluctuation in the entire process and would greatly appreciate some advice and guidance.
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Hello! Changes in skin conductance level are often estimated based on area under the curve or PP interval. This chapter might be useful: http://www.imd.inder.cu/adjuntos/article/487/Methods%20in%20Mind.pdf#page=116.
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People with disabilities are often denied the right to decide, even in basic aspects of their lives. Once in institutions, decisions are made for them, assuming they are unable. Does this have a scientific base? What are the necessary cognitive functions? What disabilities are affected? Brain damage, dementias, schizophrenia... How is it assessed? What are the criteria?
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For the past ~30 years, two rather fundamentally incompatible theories of cognition have existed side-by-side despite thousands of experimental results from fields as diverse as linguistics and systems neuroscience using everything from functional neuroimaging to analyses of classical languages. The problem isn't so much a matter of complexity. It's the vast amount of contradictory literature that, for your question, means the answer to "who is qualified to use what methods to determine whether x individual is capable of y set of cognitive functions?" depends fundamentally on who you ask. Ask Lakoff, Chao, Gibbs, Pulvermüller, etc. and you will be told that the higher cognitive function is domain-general, embodied, and intricately linked to culture, language, etc. Ask Chomsky, Pinker, Caramazza, Foder, etc., and you will be told that higher cognitive processes are domain-specific, that the mind is functionally massively modular, that it is a symbol processing machine, etc. Something as fundamental as severe brain damage that results in aphasia or similar cognitive deficits is interpreted fundamentally differently by perhaps half of those in the cognitive sciences. That's just the issue of how the mind works and what the foundations of decision-making processes are (and how they can go wrong or be improved); go into clinical issues and you are faced with fundamental disagreements over what clinical issues actually are, let alone how they relate to the divides over the nature of the basis for cognitive functions. Add to this the desire to communicate a non-existent collective body of research to political, legal, and non-profit organizations involved in mental health, institutional commitment, etc., and you are essentially taking on the question "if there were an agreement within the cognitive sciences over the nature of cognition and higher cognitive functions, then if this were translatable into a non-existent body of clinical literature sufficiently explanatory and empirically based, then how could these non-existent frameworks be combined to inform policy and policy makers who are not scientists nor equipped to evaluate scientific literature?
Alternatively, you could set your sights a bit lower. For example, it doesn't really matter if seeing one's recently departed loved one's is a cultural phenomenon that is therefore normal in one context but not another or if it is necessarily indicative of either mental disorders or poor decision making/judgment capabilities. Where it is a normative reaction nobody is going to admit someone for such behavior, and where it is aberrant the extent to which cognition is culturally-based or embodied and/or to which disorders fit the biomedical model are mostly irrelevant- such behaviors are then by definition indicative of an inability to function within society. Likewise, it doesn't matter if something as severe as multiple personality disorder/dissociative personality disorder fits a sociocognitive model or a biomedical model- being unable to remember large portions of your life because you have more than one "alter" that for all intents and purposes means you act like fundamentally different people at different times means you are incapable (again) of normative behavior, risk assessment, etc. In other words, you don't need to understand the brain so much to get to the heart of the issue. The real issue is not whether there is some scientifically valid diagnostic criteria for whether someone has a disorder that interferes with their social, cognitive, emotional, or other brain functions to such an extent that warrants removing certain rights they have over their own person. It's whether or not a person can function in the society in which they live. Like mental disorders in general, this is not a matter of criteria based upon neuronal models, neurophysiological dynamics, or even neurocognitive measures per se, but rather the much simpler question "given that we know how most people behave, and given that X individual does not conform to this pattern, are they therefore a danger to themselves and/or others? Someone who believes that the moon landing was faked, dinosaur bones were planted as part of a conspiracy, the Knights Templar hid information about Jesus' descendants, and similar theories, but who goes to work every day, pays the bills, perhaps has a stable relationship, and is neither prone to violent outbursts nor in general known to be more than "odd" by acquaintances shouldn't be committed. It could be that there are all kinds of interesting reasons underlying such a worldview, and indeed there is extensive literature on this kind of question. It's irrelevant, however. Likewise, someone habitually runs into trouble, with the law, is prone to violent outbursts, has justified harming others for trivial reasons, etc., could have be suffering from neurological damage (this goes back all the way to Phineas Gage) or from some psychiatric condition and it couldn't matter less (for treatment, it absolutely matters, but not for any evaluation of whether the individual should have the rights over their own person limited or autonomy denied).
I think you might be looking in the wrong place for the answers. Not that I don't understand the desire to take on ambitious projects, mind you, it's just that unless you personally solve fundamental divides in two sets of fields (the cognitive sciences and clinical/psychiatric sciences), you won't really have a place to start. If you do happen to solve such problems, don't tell anybody just email me the results so that I can take all the credit. :)
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What do you think is the best method for doing this (without anesthesia)?
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I'm agree with Gedeon about anesthesia. We are registering resting EEG asking children to play with us, for example like we are austronauts and we are in a dark cosmos that's why we need to close eyes and not to move before we reach our station. It takes a lot of time to make a child feel free, not everyone wants to play,etc. Better to meet 2 times and more. It is painstaking way, but if you manage to do it you feel happy, belive me. Play with a child and ask mother to help you.