Neuropsychiatry - Science topic

Hi,

Maybe some of these references are of use to you:

Kovács I, Richman MJ, Janka Z, Maraz A, Andó B. Decision making measured by the Iowa Gambling Task in alcohol use disorder and gambling disorder: a systematic review and meta-analysis. Drug Alcohol Depend. 2017 Dec 1;181:152-161. doi: 10.1016/j.drugalcdep.2017.09.023

Grassi G, Makris N, Pallanti S. Addicted to compulsion: assessing three core dimensions of addiction across obsessive-compulsive disorder and gambling disorder. CNS Spectr. 2020 Jun;25(3):392-401. doi: 10.1017/S1092852919000993

Brière M, Tocanier L, Allain P, Le Gal D, Allet G, Gorwood P, Gohier B. Decision-Making Measured by the Iowa Gambling Task in Patients with Alcohol Use Disorders Choosing Harm Reduction versus Relapse Prevention Program. Eur Addict Res. 2019;25(4):182-190. doi: 10.1159/000499709

Would a private research center be convenient for you ?

There is also a MINI for DSM5 translation to Portuguese. It is an excellent tool for clinical research.

Ali Amad

Many thanks for this - but unfortunately this version skips chapter 8 (skips from chapter 6 to 14). I can’t find it anywhere on the internet. Anne

I guess that psychosis is linked to high dopamine levels in the brain. So the psychotic phase would cause diminished self-control compared to healthy controls, because dopamine in my opinion attenuates the dACC (dorsal anterior cingulate cortex) processing and output (by predominantly D1 receptors on GABA neurons or D2 receptors on glutamatergic neurons). So too much dopamine in the system decreases the warning role of dACC, lowers worries, anxiety, caution and leads to underestimation of risks and the weight of potentially negative consequences (i.e. drink driving, random violence in pubs) during decision making.

In addition high dopamine levels would potentiate impulsivity and drive/motivation to go for the potential rewards, in spite of bad consequences (as both the inhbitory avoidance loop in ventral striatum and the cognitive self-control D2 loop in dorsal striatum are attenuated by dopamine).

High dopamine in psychosis state would also stimulate amygdala and thus processing of threat, leading to increased active avoidance and aggressivity. So the psychotic patents are less in control and more impulsive.

reference in https://www.scienceopen.com/document/vid/13e62385-1fb0-4a49-9a5d-e435ba3a5b95e?1

These articles may lead to a  conclusion.:

Dopaminergic role in regulating markers of sleep homeostasis

The Journal of Neuroscience, 8 January 2014, 34(2): 566-573; doi: 10.1523/JNEUROSCI.4128-13.2014 

Influence of Sleep and Sleep Deprivation on Ictal and ..

.

The role of sleep dysfunction in the occurrence of delusions ...

www.sciencedirect.com/science/article/.../S027273581500119...

ScienceDirect

 by S Reeve - ‎2015 - ‎Cited by 3 - ‎Related articles

Sleep dysfunction is extremely common in patients with schizophrenia. ... and psychotic experiences, particularly delusions and hallucinations. ...... the variation (63%) in high frequency EEG activity during REM sleep (Tekell et al., 2005).

... (Non Rapid Eye Movement) sleep, ... Epileptiform Activity. The effects of sleep ... a variation during sleep with typical EEG with ...

 Published in:

Epilepsy Research and Treatment · 2013

Authors:

Antonio Diaznegrillo

About:

Medical research · Bioinformatics

Regards

A group in Helsinki has a follow up study on our ERP study:

Sokka et al., Int J of Psychophysiology, 94(3), 427-436, 2014.

They included 41 burnout patients and 29 controls. PLease have a look

 http://www.sciencedirect.com/science/article/pii/S0167876014016420

Hi Matej

The literature shows that the error rate in medication administration is about 10% (not counting errors in timing). That means about 500 errors each day for a hospital with 600 beds. The reporting rates run at 200 per year which is a tiny percentage. I have come to appreciate that it is better to concentrate on those errors that are reported than to expend energy on increasing the reporting rate. Much can be learned from each error and implementing a change to prevent the error will also prevent many of the other unreported ones. In my own hospital there is a committee dedicated to analysis of error reports and making corrective suggestions. There are two doctors, two nurses and two pharmacists. Each brings their own experience and perspective to the discussions. This could be extended to the problem of inappropriate prescribing. Multidisciplinary groups are ideal and it should be implemented through each discipline with reports back to the committee. An essential part of this kind of activity is to have the full support of the management.

Regards

Here is an other interesting reference

Hello Sade, Research the Journals of Rehabilitation of TBI patients, (Not sure if that is the exact name) Research counseling journals. Visit a TBI unit in a major teaching Hospital (probably Temple U.)see what if their counseling programs are evidence-based. Howe do they measure outcomes?

Learn as much as you can about what brain areas are affected by TBI. Is it a closed head injury or one with injury exposing the brain or invading through the skull. This core information will allow you to asses theTBI's neurological sequelae. has affected the frontal lobe, which is executive functioning, and affects decision making? Some injured areas affect judgments and insight into decision-making. In some ways, the person may be viewed as Learning Disabled. Personality changes are sometimes seen. So the counseling process has to be tailored to the current level of acquisition of new learning. They have a lot to do in terms of physical and occupational rehabilitation, thus their energy is focused on that.component.

One of my patients who was well educated and highly functioning before h is TBI, from a beating, loss his ability to word-find in his conversations, had slowed speech responses and had difficulty composing sentences when in a group, difficulty making decisions on leisure activities. So he felt undervalued, lost self-esteem, and became deeply depressed. These life changes motivated him to pursue counseling, and it has been tailored to his needs, by great patience, positive regard and instillation of hope by the therapist. Cognitive rehabilitation is for someone else. to do.

Young adults have their own developmental tasks. This age group in general has attitudes about going to any kind of counseling, until they become aware of symptoms of emotional/ psychological problems and understand how they are impeding their functioning and progress in rehab. His/her greatest ally is one trusted professional that they've bonded with, from whom they may take advice.

Contact the Christopher and Dana Reeve Foundation. Information Specialist handler@christopherreeve.org. Anther wonderful resource is

Bernadette Mauro

Director, Information and Resource Services

Christopher and Dana Reeve Foundation

Paralysis Resource Center

636 Morris Turnpike, Suite 3A

Short Hills, NJ 07078

(800) 539-7309

She will talk to you at length over the phone and send you loads of information. She may also direct to further resources specifically about counseling issues in TBI.

Best of luck in studying the special needs of this population.

I hope this wasn't "too much information" than you wanted to know.

Janet D'Arcangelo

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. :)

From a grant application I submitted a while ago (based on mostly rat studies, and a few studies with humans):

DA/5-HT interaction can be conceptualized on a system and on a neuronal level. On the neuro-anatomical level, 5-HT neurons in the raphe nuclei project to DA neurons in the VTA and substantia nigra, as well as to their targets in striatum and the PFC. The clearest evidence for the influence of 5-HT on DA signaling is that lesion of the raphe nuclei leads to increased levels of DA in the striatum and to decreased DA levels in the PFC 31. This superficially straight forward picture is complicated by the complexity of 5-HT receptor influence on DA signaling, which resists a simple association of receptor type and excitatory or inhibitory function10. While the raphe nuclei also receive projections from the VTA32, projections from DA neurons to 5-HT neurons and their targets are comparatively less developed. Consistently, reports of DA influence on 5-HT function are rare, though it has been shown that stress induced changes in 5-HT signaling required an intact DA neurotransmission in the nucleus accumbens33.

On the system level, DA/5-HT interaction is thought to be involved in adaptive behavior by signaling the long-term average rewards and the value of currently available actions. More specifically, Cools and colleagues hypothesize that tonic DA and 5-HT levels signal average reward and punishment, respectively, obtained when performing an instrumental task11. These expectations are crucial for adaptive behavior because they are the basis for the evaluation of current outcomes and because net outcome expectations (average rewards – average punishments) are thought to deter-mine response vigor/inhibition10. Intuitively, the DA/5-HT interaction is thought to calibrate out-come evaluation by providing a yardstick against which outcomes can be evaluated, and by strengthening approach or avoidance behavior depending on reward expectations.

The system level DA/5-HT interaction is also apparent in a number of patient studies. For in-stance, L-Dopa medication of Parkinson’s disease can induce psychosis, and in the area of decision making increased risk taking and impulsivity by biasing the system towards stronger response vigor (due to increased tonic DA levels) and overestimation of action values (due to stronger positive prediction errors). Interestingly, selective serotonin reuptake inhibitors and the 5-HT precursor L-Tryptophan can alleviate these undesired side effects34, supporting the view that 5-HT modulates DA action. Further evidence for DA/5-HT interaction comes from a study of combined tryptophan and tyrosine depletion, which found that tryptophan and tyrosine depletion individually reduced interference in the Stroop task, but a combined depletion did not35. In animal experiments, Winstanley et al12 investigated delay aversion after modulating both nucleus accumbens DA/NA and 5-HT neurotransmission and found that either manipulation alone had a small (if any) effect on behavior, whereas a combined manipulation shows the largest effect.

This article is might answer your question too.

Hi

We just published a paper that may interest you supporting the concept that bodily Hallucinations phenomenology is linked to the cortical somatotopic organization:

About hallucinations, this book should also deeply interest you :

Jardri, R., Cachia, A., Thomas, P., & Pins, D. (Eds.). (2013). The Neuroscience of Hallucinations. New York, NY: Springer New York. doi:10.1007/978-1-4614-4121-2

No retention time but more conservatism

The problem you face is that all the commonly used models of 'depression' are not in fact models of depression but merely screens for detecting drugs with a particular mode of action - Commonly used tests include tail suspension (Steru et al 1985; Cryan et al, 2005), forced swim (Porsolt et al 1977), mouse killing (e.g. Song and Leonard, 2005), chronic social defeat (e.g. Kudryavtseva et al 1991, Keeney and Hogg 1999) and chronic mild stress (e.g. Willner et al,1987; Monleon et al 1995) but none of them have any use beyond detecting the actions of drugs that work in the same way as currently available antidepressants - that we know now to be largely ineffective in the context of the depressed population as a whole - so they are basically of no use at all - see Hendrie and Pickles 2012 for review http://www.academia.edu/2240421/The_failure_of_the_antidepressant_drug_discovery_process_is_systemic