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Anxiety Disorders - Science topic

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Hello,
I would love to receive some recommendations from experts in regards to the topic, whether there are valid findings in research on biological markers for anxiety disorders. I am trying to gain some stable insight and be able to argue in favor of the notion, that no anxiety disorder "comes from a malfunction/sickness of the brain".
Thank you in advance!
Best
Ivo
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I an looking for an resting state (eyes closed) EEG datasets for any kind of psychiatric disorder. These can include, but not limited to
  • Alcohol use disorder
  • Acute stress disorder
  • Addictive disorder
  • Anxiety disorder
  • Behavioral addiction disorder
  • Schizophrenia
  • Post traumatic stress disorder
  • Depressive disorder
  • Bipolar disorder
etc.
I would prefer if the datsets contain raw EEG data eg EDF files but. If anyone can assit i would really appreciate that. Thank you in advance
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Casodex (or bicalutamide) is available only as a racemic mixture (S and R enatiomers): 1) the pharmacologically active R (-)-enantiomer, and 2) S-Casodex, the inactive (+) enantiomer. The S-enantiomer is thus the non-working compound but is also metabolized at a much lower rate. In other word, much higher plasma levels are the result. Does anybody know if casodex can increase emotional instability/anxiety? And which enantiomer is causing this?
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Re: anxiety as a side effect of bicalutamide
THIS IS FROM WIKIPEDIA [paraphrased and abbreviated]: Side effects due to androgen deprivation include mild-to-moderate breast tenderness and enlargement in up to 80% of men, along with feminisation. Reduced body hair and muscle mass, feminine fat distribution, reduced penile length, and decreased semen volume can occur, along with hot flashes, sexual dysfunction, depression, fatigue, weakness and anemia. Bicalutamide monotherapy has also been associated with an increase in the rate of heart failure.
MY OPINION: in view of this side effect profile, depression, anxiety and id-percieved stress, in a percentage of subjects, is to be expected.
Stress-related intracellular hypothyroidism (IC), producing CFS-like symptoms including anxiety, confusion and cognitive loss, will result.
Incidentally, cardiomyopathy resulting from IC is the probable cause of the heart failure mentioned in the Wikipedia article.
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I am writing an essay on probiotics and faecal microbiota transplants etc. I am proposing a new treatment for generalised anxiety disorder exploiting the gut microbiome. I have to answer a question saying what is the biggest challenge for this.
I believe the answer is something like that all species are not currently culturable and that we don't even know all the species in the gut microbiome. Any further ideas?
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The current treatments that we have are mainly focusing on altering/causing a shift in the microbiome by the supplementation of probiotics, prebiotics, and postbiotics. Despite being popular, these treatments are not always useful and their beneficial effects are hard to detect.
Furthermore, we still don't understand fully the relationships between different bacteria and the way they interact in a complex matrix such as the gut.
Furthermore, pathogenic species of bacteria express their genes differently based on the environment they are found in. So understanding how they interact with other bacteria is key here to form a microbiome-based treatment.
Therefore, until we have a complete picture of the microbiome on a strain level and how these bacteria interact together or with their host, we won't be able to form novel microbiome-based treatments
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I am interested in learning more about the current state of research in this area.
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Here are some relevant links for your ref:
(1) The relationship between alexithymia, defense mechanisms, eating disorders, anxiety and depression: https://www.rivistadipsichiatria.it/archivio/3301/articoli/32715/
(2) The association between depression and anxiety in adolescent females:
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There is a protective role of estradiol against fear overexpression during the recall of fear memories, but why are anxiety disorders more common in females?
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I agree with all answers
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hello everyone, I have just entered my Ph.D and I am interested in alexithymia and its link with anxiety disorders. For this research I need recommendations for self report functional assessment questionnaire, which I can use on both populations to assess if they face any difficulties in their functioning.
THANK YOU
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The Outcome Questionnaire-45 might be helpful for both clinical and non-clinical populations. https://www.oqmeasures.com/oq-45-2/
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What is the impact of the lockdown on the emotional stability of involuntarily childless women in abusive marriages.?
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تاثير سلبي
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Can you tell me "what are the different clinical stages of Mental Health among young boys. " Related to anxiety or depression...If so can you plz tell me those stages.
E. G
Stage 1
(a)
(b)
(C)
Stage(2)
Stage (3)
Stage (4)
Stage (5)
Stage(6)
----++++--
What are the characteristics of these stages?
How as a clinical practitioner do you define these characteristics.?
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As already indicated, the STAGES, according to the Natural History of both psychoptologies, would be AND IT IS unethical and antimoral to see how they appear and evolve WITHOUT INTERVENING IN THEM !; But the LEVELS or DEGREES or STAGES of SEVERITY are universally categorized or hierarchical, from less to more, as: a) ABSENT, b) MILD, c) MODERATE and d) SERIOUS -which is how they are hierarchized, for example, the BDI -Beck Depression Inventory- and BAI -Beck Anxiety Inventory-
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I study and research about anxiety disorders in children in Iran and I sometimes face questions like this and unfortunately I could not find article or book to answer that.
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"COGNITIVE BEHAVIORAL TREATMENT FOR CHILDREN WITH ANXIETY". Children learn to handle the bully in their brain; by Jerry Bubrick, PhD; INSTITUTE MENTE INFANTIL (and II):
"Related: Do's (and Don'ts) When Kids Are Anxious
It is also important to help children really understand how anxiety is affecting their lives. In fact, I sometimes map the things a child cannot do because of their fears, like sleeping in their own bed, going to a friend's house, or sharing meals with their own family, and how that makes them feel. . It is important to make children understand how their anxiety works and to gain their trust because the next step, facing their fears, depends on their trust in me.
Exposure therapy slowly and consistently helps a child cope with her fears.
Adopting Robert Frost's observation that "the only way to get over a situation is to get through it," exposure therapy helps a child slowly and consistently cope with his fears so that he can learn to tolerate his anxiety until it subsides, eventually Instead of reacting by seeking comfort, escaping, avoiding, or performing rituals such as hand washing.
How does exposure therapy work?
The first step is to identify your triggers. We design a "hierarchy of fears," a series of escalating challenges, each of which is tolerable, and which together build significant progress. Instead of thinking in terms of black and white (I can't touch a dog or I can't cross a bridge) the children are asked to think in levels of difficulty. We could ask a child with a fear of contamination, for example: “On a scale of 1 to 10, how difficult would it be to touch the door handle with one finger? Knock and open the door?
Related: How Anxiety Leads To Conflictive Behaviors
For a child with a fear of vomiting, we might ask: “How difficult would it be to write the word vomit? If that's a 3, then let's say saying 'I'm going to vomit today' could be a 5. Watching a cartoon of someone vomiting could be rated 7. Watching an actual video of someone vomiting could be a 9. On top the hierarchy would probably be eating something that the child thinks will make him vomit. By rating these various fears, children come to realize that some things are less extreme, and more manageable than they thought.
Then we expose the child to the trigger in its mildest possible way, and we support them until the anxiety subsides. Fear, like any sensation, fades over time, and children gain a sense of mastery as they feel the anxiety diminish.
Intensive treatment
With a child who has severe anxiety, who can barely, for example, leave his room for fear that his parents will die, or who has to wash his hands dozens of times a day to avoid contamination, it can work to work with him several times a week, for several hours per session. We do exposure therapy in the office, and when a child is comfortable enough, we do it outside. For someone with social anxiety, for example, we could go outside wearing funny hats, or walk with a banana tied with a rope. For someone who is afraid of pollution, we could get on the bus together, or shake hands with strangers and then eat potato chips without washing our hands.
Once we have worked with some exhibitions, and the child feels more secure, I assign homework to practice what we did in the sessions at home. We want the kids to really master the exhibits before moving on. And parents are taught to help children thrive by encouraging them to tolerate feelings of anxiety, rather than running to protect them from their anxiety.
Treatment for mild to moderate levels of severity usually requires 8 to 12 sessions, and some children make more progress if they are also taking medications to reduce their anxiety, which can facilitate their involvement in therapy. It is important to understand that exposure therapy is hard work, for children and parents. But as the fear subsides, the children go back to doing the things they love to do, and the family welcomes back a child they feared they had lost, and that is a great reward".
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There are dozens of studies that investigate the effect of tdcs on depression, but not on anxiety (generalized anxiety disorder).
I have found two randomized controlled trials, and two case studies. (studies that perform multiple sessions, there might be more of them but still much less than depression studies)
This is strange since anxiety disorders have a higher prevalence than depression, and are also quite debilitating.
What explains this relative lack of studies ? Might it be that tdcs is not very effective in this disorder so that studies that fail to find an effect don't get published ?
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Hi Victor,
maybe these articles will help you :)
Kar, S. K., & Sarkar, S. (2016). Neuro-stimulation Techniques for the Management of Anxiety Disorders: An Update. Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology, 14(4), 330–337. https://doi.org/10.9758/cpn.2016.14.4.330
de Lima, A. L., Braga, F. M. A., da Costa, R. M. M., Gomes, E. P., Brunoni, A. R., & Pegado, R. (2019). Transcranial direct current stimulation for the treatment of generalized anxiety disorder: a randomized clinical trial. Journal of affective disorders, 259, 31-37.
Stein, D. J., Medeiros, L. F., Caumo, W., & Torres, I. L. (2020). Transcranial direct current stimulation in patients with anxiety: current perspectives. Neuropsychiatric Disease and Treatment, 16, 161.
Clarke, P. J., Sprlyan, B. F., Hirsch, C. R., Meeten, F., & Notebaert, L. (2020). tDCS increases anxiety reactivity to intentional worry. Journal of psychiatric research, 120, 34-39.
Heeren, A., Billieux, J., Philippot, P., De Raedt, R., Baeken, C., de Timary, P., ... & Vanderhasselt, M. A. (2017). Impact of transcranial direct current stimulation on attentional bias for threat: a proof-of-concept study among individuals with social anxiety disorder. Social cognitive and affective neuroscience, 12(2), 251-260.
Kind regards
Pavla
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I've used Marteau & Bekker's (1992) six item state short-form of the State-Trait Anxiety Inventory (STAI) in a pre-op anxiety study and I was wondering if there are any established cut-offs that are available in the literature that I might have missed?  For example, to demonstrate low, moderate and high anxiety levels or to show clinically significant anxiety?  Or any established pre-op 'norms'?  Thanks in advance for any info!
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and even Andras is shortening it to STAI-5
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I want to know, if words in tables are added into the total word count of 6000 words in the Journal of Anxiety Disorders. Thank you!
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Manuscripts based on original research are limited to 6000 words of main text (i.e., not including cover page, Abstract, and references) and reviews, meta-analyses, and theoretical treatises will be limited to 8000 words of main text. Tables and figures will be limited to 5 each, regardless of manuscript type. Longer manuscripts may be considered on occasion where there is a strong and compelling rationale supported by editorial pre-approval.
Based on this instruction I do not think that the words in tables should be included in the 6000 words.
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Fear and anxiety disorders are come in children and are directly affected affected by the environmental condition (parents reaction, peers, media).
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I guess, it depends on the atmosphere that they are belonging to. Children, always, in all situations, are the reflection of their own other family members. Those are the main effectiveness of children at home. For kids, staying home orders are slightly a "Mess", and nonsense. So, as we are dealing with such pandemic, we have to keep an eye on them, ALWAYS. THAT MATTERS FOR SURE.
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The style life would be a good argument for the anxiety disorder. The events stressful and the environment involved in the process of child care could be interrelated for the development of anxiety, panic's trastorns and the physical illness. Is enough the investigation about this?
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I've seen at symposia that some people have success recruiting for research studies on subreddits like r/depression or r/anxiety. Does anyone have experience with this? I have an upcoming study where I think this recruitment method would be useful. Has anyone run into IRB issues with this recruitment method? If you've had success with this recruitment method, how did you go about making your posts?
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I've used the "subreddit" r/samplesize for recruitment, its dedicated directly for this purpose (instructions on how to post, etc., are contained in the sidebar). I got about 200 participants in of a month using this approach, and my IRB did not ask any questions.
I think posting recruitment ads on other subreddits (related to disease states, etcc) is at the discretion of the moderators. I asked about one and was told no.
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I'm working on a Project where i want the participants to only fill the survey when they're are in a state of anxiety or panic to get the most accurate answers about how they feel about certain designs.
Ethically, this seems very wrong. How can i get the results which are truest to real life scenarios to determine what works in ?
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If you are in a panic attack you probably do not go to the computer to fill in a form.
You can administer Beck anxiety inventory (BAI) and people can fill in all the symptoms they experience, I am sure they remember the symptoms well after some attacks.
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I am designing the assessment protocol of a randomized controlled trial in which we plan to include patients with anxiety disorders and I am not sure whether the GAD-7 is an adequate measure to include/exclude participants. Even when it is used as a generic measure in many trials to select patients with anxiety disorders, my impression is that the items focus too much on generalized anxiety disorder. Any thoughts about this?
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Dear Dr Gonzalez-Robles,
Anxiety disorders are a large group of different disorders with their on symptomatology, short and long term course. If you plan to include patients with different anxiety disorders in your trial, I suggest to use the MINI (International Neuropsychiatry Interview) for DSM5 for diagnosis and the HAMA (Hamilton Scale for Anxiety) and CGI (Clinical Global Impression ) for severity. They could be in your inclusion/exclusion criteria.
Best
Antonio
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We prescribe isotretinoin in many cases of acne vulgaris specially nodulocystic acne and in a few other diseases. Isotretinoin has many adverse events like depression, emotional lability, suicidal ideation, anxiety disorders and so on. We should screen a patient for psychiatric adverse events during each follow up visit who is on isotretinoin therapy. Are you in favor of screening? What screening tool should we use? Why these psychiatric events develop?
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Harasit Kumar Paul , very good question. I hadn't thought of this, but I have seen this happen a lot clinically (symptoms of psychiatric illness secondary to isotretinoin therapy)
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I am in urgent need of participants as I'm still someway from my target. Any completions will be much appreciated.
I am studying a masters in Clinical Psychology and my study is investigating how a range of disorders that are commonly associated with each other may be interacting as a network (disorders such as anxiety, depression, ADHD, autism, panic disorder etc.).
The questionnaire is roughly 30 minutes but can be done quicker. There is also a draw for £20 amazon vouchers per 50 participants. Thank you.
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I've done the first part of the survey, good luck with your project! However, the inquisit part at the end doesn't work - the error said something to do with the licence and that it would not run.
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One would expect equally interesting results in depression. Do you limit your focus on anxiety disorders because the role of emotional arousal has already been investigated in depression therapy?
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Hi Ingmar,
Thanks for asking! Actually, the scope is limited to anxiety disorders simply because they portray my research interest and expertise. If you are interested in research on vocal parameters in depression, I would be happy to send you some articles!
Best, Gesine
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Does anyone know interesting articles about the effects of relaxation trainings on anxiety disorders? I focus on general anxiety, but also specific anxieties can be interesting
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Anxiety plays the very disturbing parts according to the nature problem & to me this implies from small category person to the higher level of person .
It is in this line sometime back I have expressed my views
Anxiety depend on the nature of every individual person depending upon the problem & the period for which they have to pass . In case of individual certain person are wide powerful in their individual sensitivity & they are facing problem as it come believe in that we have to cooperate with the inevitable .
As we know which well many person they have to pass their various phase of their disturbing problem of the life . Children problem ,illness & death in the family ,difference with the member of the family ,illness calling for long waiting period with the use experiences,disturbing illness like Cancer, death of the husband or wife ,are the problem which remain the part of anxiety for such long duration & this can be avoided only with the passage of time .
This is my personal opinion
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NAMI estimates that 8% of children and 18% of adults have anxiety disorders. Anxiety disorders impair test performance. Good test performance is a gateway into better career paths (college students make about a MILLION dollars more in a lifetime, than non-college students., STEM career folks make about 10,000 dollars per year more than their non-stem colleagues). Providing test-taking accommodations would give those disabled by anxiety, a chance to show what they know, under less stressful exam conditions. Have you known anyone with severe test anxiety (a social anxiety disorder) who chose a less rewarding path because of the fear of exams? Dr. Ron Rubenzer. Fellow- American Institute of Stress
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As a practitioner at the secondary level, 504 Plan accommodations for state testing was limited to 'extended time' and 'quiet space'. By the time I left the classroom in 2016, it was getting harder to get accommodations for students with anxiety disorders under 504 Plans. As the student population increased it was also harder to find facility space to meet the above accommodations.
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The point of discussion is that how far a patient with symptoms of agitation and restlessness due to Generalized anxiety disorder would harm his/ her family members. Do you think that the times of agitation could be considered Panic attacks? the same inquiry is still. To what extent panic attack is attributed to dangerous behaviour against family members.
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While there may be research showing that individual's with GAD or social anxiety disorder exhibit more anger, I have never run across this in my own life. I have dealt with GAD, Social Anxiety, and Panic Attacks for over 40 years now. If anything, and this is related to only my own experiences and friends who have dealt with the same issues, those of us with social anxiety (especially) tend to retreat rather than react. During a panic attack, a true, certified panic attack, there is absolutely no time or opportunity to show anger or violence. Panic attacks are all consuming and if there is ever a moment where it is "all about me", it is during a panic attack. For example, I pray that nothing dangerous happens to someone I love during one of my panic attacks because I simply would not be able to respond to it. Social Anxiety, in my case again, led to 2 years of agoraphobia because I chose to go off of my medication. Even after being back on my medication for over 2 years now, if there is a line at Walmart and it doesn't move fast enough, I will first kneel down. If after kneeling for several minutes it is not yet my turn to check out, I will simply leave my cart and go home. Those I know who have dealt with either social anxiety or generalized anxiety tend to have similar reactions, although perhaps not as exacerbated. I guess what I am trying to show by the examples I have given, is that I do not see aggression and anger being part of anxiety UNLESS the person has a co-morbid issue involving either a secondary psychological disorder or a substance abuse disorder. I hope this helped a little!
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I know there is (somewhat) widespread agreement that relaxation techniques can be used as a form of avoidance of exposure in panic disorder, and hence breathing techniques and progressive muscle relaxation are discouraged so that the client feels the full physiological activation and becomes aware that the symptoms that he/she experiences are not actually dangerous or life-threatening in any way.
However, I was wondering whether this would apply as well to exposures in other forms of anxiety, say, specific phobia or social phobia. In those instances, it seems to me that the exposure to the phobic stimulus is not prevented by the relaxation/breathing techniques, and so these techniques would be merely an aid to facilitate the exposure. The client would not habituate to the physiological activation (which would be dampened by the relaxation techniques), but he/she could still dispel his/her irrational beliefs about coming into contact with the feared object.
Any science to back this up?
Cheers!
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Marc Josep Garcia Hervás that sounds like an interesting idea! And I suppose it would depend on the ultimate aim- to eliminate distress or manage more effectively?
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Dutch psychiatrist Henricus Cornelius Rumke defined a term "Praecox Gefuhl" meaning Praecox Feeling to indicate the phenomenological experience by the clinician in first few minutes of encounter with a schizophrenic patient, in order to reach a diagnosis. Though the topic is less considered in mainstream psychiatry currently, but many proponents of phenomenological approach favor the existence of such a feeling.
From the similar perspective, are there any other feelings that clinicians experience in encounters with other kinds of patients like personality disorders, or OCD or depression, or anxiety disorders? And for that matter, even childhood disorders too like autism or ADHD. I am looking for some relevant literature as well as personal experiences of clinicians, since I believe that such phenomena have not been reported often. Please share your own experiences too.
P.S. This question arose from a personal experience of a feeling of "being possessed" during the first few minutes of interviewing with a patient diagnosed with Narcissistic Personality Disorder having other Cluster B traits. I labeled this feeling, similar to Rumke's as "Gefuhl Besitz", which means "feeling possessed". I have experienced similar respective feelings with depressed/manic/OCD/Borderline personality and other patients too. There have been many repeated experiences of these feelings, quite often, which follow a pattern corresponding to similar diagnoses. That's why I am curious!!
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This answer reflects my experiences in 15 years of actual nearly full-time clinical practice. I believe these are the sorts of answer you were pursuing?
1) There are times that walking into the hospital room of a patient who is severely depressed feels as if there is a palpable gust of "sad" that "comes off" the patient (this is not literal of course). I have described this experience over the years to students and trainees as similar to the actual gust of heat one feels when opening the door of an oven that has been at 400 F for a while.
2) I think we can all universally agree there are some persons with Autism you meet and it's completely clear immediately - by this I mean the sort of classic, profound Autism characterized by a person being non-verbal, lacking joint attention, and engaging in repetitive, self-stimulatory behaviors. When people say they "just know" someone has Autism without doing a complete diagnostic short of those sorts of presentations, frankly I get concerned.
3) As for ADHD, many times you will see behaviors from a child that could have you immediately conclude that the child must have it, until you take a history that includes significant trauma. So that immediate feeling is not trustworthy at all, and because it can be strong, has to be actively fought against.
I'm sure there are other similar phenomena if you were to ask people who do a lot of clinical work. I believe that all of this is what is intended to be captured under the concept of transference. But that does not mean it isn't possibly worthy of more careful description and understanding than lumping into one big pot.
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Could someone help me with this question.
I have had several final year students on their BSc in Psychology wanting to use Zung Self-Rating Anxiety Scale.
I have seen many places on the web in journals, own websites with the information that came from the original ref
Zung WWK. A rating instrument for anxiety disorders. Psychosomatics. 1971;12:371–379
This is fine even Wiki has it mentioned.
However as the author has died (1992) the old way to get guaranteed permission seems through the APA website, but this portal seems totally unfriendly and unusable.
Can anyone give a better answer to how I can establish if our students use this scale it would okay to simply have the original reference it came from?
I have tried to contact the different websites on APA for permissions but nothing has been forthcoming from them.
Looking forward to light at the end of tunnel
Kind regards
Mr Peter Beaman BSc FHEA MBPsS
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As the questionnaire was actually published in the journal, i.e. one can simply copy the questions from that, this would usually be considered as in the public domain. Although some organizations may be selling copies of the scale, I doubt they have any right to claim copyright. They may be able to claim some rights to their actual copy, in their particular design layout, but not for the questions. In short, you could just make your own copy from the questions listed in the article.
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DNA structure and activity can change with environmental factors. But does experience such as sexual abuse create significant biological effects on DNA?
These type of researches are so important in detecting crime.
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Just like environmental factors, psychological factors may have an impact on gene expression and its regulatory mechanisms but the extent of impact would be depndent on multifactorial aspects and would need to be ascertained in a case to case basis.
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I am wanting to do a study on the identification and treatment of children with anxiety disorders in the school setting. What is the best type of method to use? I was considering the case study, as the sample will be 10 children. Is there a more suitable method to use?
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As a special education teacher and person with anxiety disorder, I found the ACE-Adverse Childhood Experience studies of 1995-97 to be both professionally and personally helpful to me and my research. It found that many psychiatric challenges result from traumatic events in early life, including drug and alcohol use and addictions. Left untreated these experiences can lead to severe physical illnesses and possibly early death. I support your efforts in studying this topic and suggest a qualitative study because you have a small sample which will allow a deeper study of the children as some children will need more time to develop trust and provide fear-free answers to your research questions.
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If inflammation plays a part in the cause of psychiatric disorders--what might be causing the inflammation to begin with?
& Pre-diagnosis and post-diagnosis use of common analgesics and ovarian cancer prognosis (NHS/NHSII): a cohort study. https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(18)30373-5/fulltext
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Dennis Mazur thanks for sharing. I agree that the field of immunology is complex, and I'm confident as we ask more questions and do more research, we will find more answers. Some will take longer than others.
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Needs to be fairly short and accessible. Preferably relating to MH in children but that's not essential.
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Hi,
Maybe this questionnaire can help.
Best wishes
Yaakov
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About one in five people have some fear of flying or aviophobia. In most cases it makes flying an uncomfortable experience.....
For more severe cases, where the panic begins hours or days before a flight and can even lead to avoiding flying altogether, hypnotherapy or special flight courses have been known to help.
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DASS (Depression Anxiety Stress Scale) -21, a validated screening instrument.
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Cut-off scores very much depend on the population from which you are sampling. Attached is a very general suggestion.
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I am finding it difficult finding studies specifically looking at the mental health consequences (good or bad) that come with being adopted, espicially at a young age. My psychiatrist told me that adoptees are much more prone to things like: anxiety disorders, mood disorders, and substance abuse. I would love to find literature that supports this statement (I do not doubt my psychiatrist, I'd just like to see the studies making these conclusions).
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There are a lot of excellent epidemiological studies with massive sample sizes using the comprehensive Scandinavian Population Registers. In fact, I tend to doubt any social science finding unless confirmed in such samples.
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 Does there need to be a genetic predisposition to obsessive-compulsive disorder in order for trauma to trigger OCD in someone? Is there a distinction between trauma-induced OCD and OCD that is not trauma-induced other than the trigger?
Thank you!
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OCD is similar to many other psychiatric disorders in that the manifestation of the 'symptoms' are incredibly heterogeneous. For example there are 636,120 different ways to have post traumatic stress disorder based on current psychiatric diagnosis, and there are so many ways that psychotic symptoms can be combined that it makes it nonsensical to consider these as discrete disorders. Therefore it is incredibly unlikely that there is a simple genetic explanation for these complex and multi-faceted disorders.
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Researchers report 20% of Mensa members, with an IQ of 130 and over, have a diagnosed anxiety disorder, compared to 10% of the general public.
Due in part to this increased awareness of their surroundings, people with a high IQ then tend to experience an overexcitable, hyperreactive central nervous system.
More,
Hyper Brain, Hyper Body: The Trouble With High IQ
📷NEUROSCIENCE NEWSOCTOBER 10, 2017
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The society of people assesses the outstanding abilities of personalities in their Creativity. The criterion of genius is the real creations of Human, the novelty and genius of the newly created. At the same time, intellectual tests go to the background. Such tests are a kind of reference point for judging the potential intellectual abilities of a person. But a person is judged by his Creations, and not by intentions to create something unusual.
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Lots of superstitions seem to feature a sort of 'if X, then Y' sort of thinking, linking two unrelated things (If you break a mirror, you have bad luck for seven years) as well as taking nonsensical actions in order to prevent disaster (if you knock on wood three times after saying something aloud, you can prevent a 'jinx'). I've noticed that these lines of thought seem similar to those that occur within people who have been diagnosed with obessive compulsive disorder. How is thinking that knocking on wood three times in order to prevent a jinx different than thinking you have to walk around your house three times to prevent it from catching fire while you sleep? 
I assume that the separation must be more than just 'one is commonly accepted'. Is it simply that in order to be diagnosed OCD, it has to have a profound negative impact on one's life? Is an obsession with these sort of superstitions a sign of OCD?
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To Beatrice: Checking whether the frontdoor has really been closed is a trivial job with an easy to check result: yet a part of the OC patients cannot become convinced. Looking whether you have extinguished the light is as simple job: yet a part of the OC patients have to return to the room time and again to see whether they really did. In due time they may not even be able to convince themselves when they are still in the room, which is already dark. Etc.
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QBI researchers state that "Disrupted connections in the amygdala, an ancient part of the brain, are linked to depression, and anxiety disorders such as PTSD" (https://qbi.uq.edu.au/article/2017/08/emotion-processing-region-produces-new-adult-brain-cells). Interested in knowing whether any human study  exist/published that show such evidence?
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Dear Hari, Dear Colleagues,
This is an interesting question. I think the following papers will help you:
Sladky R, Höflich A, Küblböck M, Kraus C, Baldinger P, Moser E, Lanzenberger R, Windischberger C. Disrupted effective connectivity between the amygdala and orbitofrontal cortex in social anxiety disorder during emotion discrimination revealed by dynamic causal modeling for FMRI. Cereb Cortex 2015;25(4):895-903. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4379995/pdf/bht279.pdf
Chase HW, Moses-Kolko EL, Zevallos C, Wisner KL, Phillips ML. Disrupted posterior cingulate-amygdala connectivity in postpartum depressed women as measured with resting BOLD fMRI. Soc Cogn Affect Neurosci 2014;9(8):1069-1075. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4127008/pdf/nst083.pdf
Ramasubbu R, Konduru N, Cortese F, Bray S, Gaxiola-Valdez I, Goodyear B. Reduced intrinsic connectivity of amygdala in adults with major depressive disorder. Front Psychiatry 2014;5:17. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3928548/pdf/fpsyt-05-00017.pdf
Liu W, Ge T, Leng Y, Pan Z, Fan J, Yang W, Cui R. The Role of Neural Plasticity in Depression: From Hippocampus to Prefrontal Cortex. Neural Plast 2017;2017:6871089. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5299163/pdf/NP2017-6871089.pdf
Hahn A, Stein P, Windischberger C, Weissenbacher A, Spindelegger C, Moser E, Kasper S, Lanzenberger R. Reduced resting-state functional connectivity between amygdala and orbitofrontal cortex in social anxiety disorder. Neuroimage 2011;56(3):881-889. https://www.researchgate.net/publication/50225446_Reuced_resting-state_functional_connectivity_between_amygdala_and_orbitofrontal_cortex_in_social_anxiety_disorder
Dong Hoon Oh. Traumatic Experiences Disrupt Amygdala – Prefrontal Connectivity. Chapter 13 from the book “The Amygdala - A Discrete Multitasking Manager”. Edited by Barbara Ferry. 2012:325-338. https://cdn.intechopen.com/pdfs-wm/41582.pdf
Leal SL, Noche JA, Murray EA, Yassa MA. Disruption of amygdala-entorhinal-hippocampal network in late-life depression. Hippocampus 2017;27(4):464-476. http://onlinelibrary.wiley.com/doi/10.1002/hipo.22705/abstract;jsessionid=F4D28266BE74122CBA0EE06241721308.f03t02
Greening SG, Mitchell DG. A network of amygdala connections predict individual differences in trait anxiety. Hum Brain Mapp 2015;36(12):4819-4830. https://sites01.lsu.edu/faculty/sgreeninglab/wp-content/uploads/sites/98/2015/11/Greening-Mitchell-2015-A-network-of-amygdala-connections-predict-individual-differences-in-trait-anxiety.pdf
Wang F, Kalmar JH, He Y, Jackowski M, Chepenik LG, Edmiston EE, Tie K, Gong G, Shah MP, Jones M, Uderman J, Constable RT, Blumberg HP. Functional and structural connectivity between the perigenual anterior cingulate and amygdala in bipolar disorder. Biol Psychiatry 2009;66(5):516-521. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2830492/pdf/nihms175753.pdf
Gee DG, Humphreys KL, Flannery J, Goff B, Telzer EH, Shapiro M, Hare TA, Bookheimer SY, Tottenham N. A developmental shift from positive to negative connectivity in human amygdala-prefrontal circuitry. J Neurosci 2013;33(10):4584-4593. http://www.jneurosci.org/content/jneuro/33/10/4584.full.pdf
Best wishes from Germany,
Martin
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I'm wondering if anyone has any experience using standardised measures of satisfaction in mental health treatment research, ideally within anxiety disorders and ptsd, please?  I'd like to introduce a valid, standardised measure to a phase III trial I'm working on.
I'm interested in the Treatment Acceptability and Preferences measure (TAP), however I can't seem to find it on the web.  I've also seen references for a Treatment Acceptability/Adherence Scale, but also can't find that.  Can anyone point me to these measures, please?  I'm also interested in the Client Satisfaction Questionnaire which I can access, but have no experience using.
Any advice would be much appreciated.
Many thanks,
Natalie 
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Hello Mary,
That's really helpful, thank you.  I will contact the authors and take it from there.  Your help is much appreciated!
Best wishes,
Natalie
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I have two problems: 1) it is somewhat hard to produce long set of negative and neutral words which will be matched in arousal, frequency and length 2) repeating shorter set of words couple times will cause habitation of stimuli.
I am wondering if you know any study or have some experience with such problems? I will be grateful for any advice.
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Yes, thats right. I don't have access to the APA site so it was helpful to find the paper on Researchgate. Paul
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I am looking for relevant research papers.
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It would be worth looking at Eleanor Maccoby's "The Development of Sex Differences" (1966) - especially the chapter by Lawrence Kohlberg.  It will give you the base literature on child sexuality and the social context/mediators which are involved.  Fairly easy to find in libraries/on-line bookshops 2nd hand.
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Development of Social Anxiety Disorder Secondary to Attention Deficit/Hyperactivity Disorder (The Developmental Hypothesis)
Social anxiety disorder (SAD) may develop secondary to childhood attention deficit/hyperactivity (ADHD) in a subgroup of the patients with SAD. Patients pass through a number of identifiable stages of developmental pathways to SAD as they grow up. Patients with ADHD have maladaptive behaviours in social settings due to the symptoms of ADHD. These behaviours are criticized by their parents and social circle; they receive insults, humiliation and bullying. After each aversive incident, the individual feels shame and guilt. A vicious cycle emerges. The patients then develop social fears and a cognitive inhibition that occurs in social situations. The inhibition increases gradually as the fear persists and the individual becomes withdrawn. Patients start to monitor themselves and to focus on others' feedback. Finally, performative social situations become extremely stimulating for them and may trigger anxiety/panic attacks. If this hypothesis is proven, treatment of 'patients with SAD secondary to ADHD' should focus on the primary disease.
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Our hypothesis was published in the Journal of Early Intervention In Psychiatry.
We describe a prodromal period consisting of three stages. Every year millions of children around the world develop social phobia (from ADHD to social phobia). Social phobia can be captured in the prodromal period and treated. Just as cancer patients captured during the period of pre-cancer (such as metaplasia, dysplasia), social anxiety can also be captured and treated in early stages. Now we are working on a scale to describe the period of Presocial anxiety.
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A premature child currently aged 1 year with severe Gravitational insecurity, vestibular hypersensitivity and oral hyposenstivity. What are the possible ways to tackle his anxiety so that he performs better in his therapy sessions
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At that age I have found  that  working through a  loved care taker  and working gently and  directly with with the gravitational insecurity  can change that situation fairly quickly,,, and the anxiety goes away and development unfolds.    Behaviors resulting from sensory issues can sometimes look like autism. However sometimes the sensory issue is the issue.  I believe I provided a vignette in my article on Consultation in Early Intervention  that is posted on Research Gate.  An occupational therapist using a sensory integration approach  to sensory processing disorders would provide the intervention that would be most effective.
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Online programs for clients to complete at home would be helpful. Articles would also be helpful. Thanks in advance.
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This is a good program that children can complete at home. It's from Phil Kendall, referenced in some previous responses. I believe there is also an analog for older children.
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I am specifically interested in instruments (e.g. questionnaires or scales) which primary school children could reasonably be expected to use with their peers.
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Thanks for your suggestions, Beatrice.
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Hello,
I want to do study on patients with  anxiety and depression. Could anyone suggest me good Neuropsychological test and stimuli tasks for EEG?
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To the best of my knowledge as a former EEG researcher, the EEG does not produce a reliable way to measure anxiety. As you may know, the EEG reflects only that part of the brain's electrical functioning that can cross the rather nonconductive skullbone. In addition, it reflects only a weak vector summation of millions of synapses. Finally, the signal is masked by the blood vessels of the head, large and small, which conduct various electrical signals (including Alpha waveforms) much better than bone due to their being filled with blood, which is electrically conductive due to its salt content.
While there is much controversial or fringe research that shows various EEG effects as a result of meditation, anxiety, and even thinking and task-solving, none of this research, to the best of my knowledge, is part of accepted medical knowledge. It cannot as yet be considered fact.
If you want a reliable measure of anxiety, you cannot do better than the State-Trait Anxiety Inventory for Adults (STAI Form Y), available at http://www4.parinc.com/Products/Product.aspx?ProductID=STAI . This is an accepted psychological instrument, having itself been validated in various human populations.
Research involving a measurement of anxiety that is based only on EEG readings may have only limited acceptance due to its dependence on the unreliability and lack of validation of the EEG as a measure of anxiety, to the best of my knowledge.
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I am a PhD student in Ferdowsi University of Mashhad in Iran. I'm studying on reflective functioning in parents of children with separation anxiety disorder. I need to preventive programs of reflective functioning for parents. I need to full preventive programs of reflective functioning.
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While buspirone, venlafaxine, and duloxetine all help with generalized anxiety disorder, for patients in whom either efficacy is limited for these agents or side effects are not tolerable, additional options are needed.  While there is some work suggesting pregabalin is also anxiolytic, I have not had good results with it so am seeking guidance re: dose, what time(s) of day to administer, and any other tips from colleagues who have had salubrious results.
Lewis A. Opler, MD, PhD
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Dr. Sood - Since Lewis put this question in the realm of *anecdotal* evidence as well as traditional EBM/PCT etc, I would note some serious downsides to the atypical antipsychotics, which I'm sure come as no surprise to you (1) pts generally report dissatisfaction with the "feeling" of olanzapine, quetiapine, and risperidone as compared to that of BZDs (most preferable) and pregabalin (next most preferable) - while they certainly have therapeutic value, the atypical antipsychotics are disliked by many patients, and thus result in much lower adherence -- they control anxiety at a cost generally not attributed to gabaergics.  (2) The jury is still out on the risks of permanent dyskinesia from all three atypical mentioned -- little research here, but litigation aplenty.  For *some* patients, I agree that atypicals can be used to manage anxiety.  For many, and ANECDOTALLY, for very high functioning pts, the "downside" to the atypicals outweighs the "upside".  That is why I think PGN, as a weaker (less addictive, less dependence-forming) gabaergic, has so much promise - it is well-tolerated, has high adherence, and as your quote states, seems to be effective in keeping pts from "relapsing" (either to BZDs or to GAD or both) after they are weaned from BZDs.  I would also suggest looking at the extensive literature on gabapentin, which I believe has a similar mechanism of action as PGN but is even weaker.  It may be appropriate for some pts with GAD and or BZD dependency.  
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Serotonin (5-hydroxytryptamine, 5-HT) is a chemical found in the human body.It carries signals along and between nerves - a neurotransmitter. It is mainly found in the brain, bowels and blood platelets.Serotonin is thought to be especially active in constricting smooth muscles, transmitting impulses between nerve cells, regulating cyclic body processes and contributing to wellbeing and happiness.Serotonin is regarded by some researchers as a chemical that is responsible for maintaining mood balance, and that a deficit of serotonin leads to depression.
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Several lines of evidence implicate decreased serotonergic activity in anxiety and major depression, but its importance in the etiology and severity of these disorders remains unclear. Acute tryptophan depletion studies support a role for decreased serotonin in depression, or at least in relapse of recovered depressed patients. Imaging and post-mortem studies indicate altered activity of discrete regions within the prefrontal cortex (PFC) and their atrophy are associated with depression. Genetic polymorphisms in serotonin genes [e.g., 5-HT transporter (5-HTT), 5-HT1A receptor] have been associated with depression, but these associations are weak and not always reproducible, suggesting that serotonin may be a predisposing factor rather than a cause of depression or anxiety. Pl. refer following thread for further details:-
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what is the best methods for conversion of primary amine to corresponding NCS?
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Moving is often described as one of the major risk factors related to affective and anxiety disorders. In my clinical practice I have found it sometimes as well, but, could be the eventual loss of space the clue of this kind of stress? Is there any statistically significant difference between depressions after moving to a bigger or smaller house?
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Change in residence and change in living conditions rank pretty high in the Holmes and Rahe Stress Scale of life events that produce distress. The effect of size would, I think, depend on its symbolic meaning - smaller size  a sign of declining social status perhaps for some or of children leaving home for good; for others small size may be welcomed - less to clean, fewer house guests, an opportunity to get rid of useless baggage........
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I am particularly interested in any studies in this field in relation to widening participation. I am currently writing a paper exploring whether Connectivism equates to inclusivity, through the lens of widening participation, and this is one particular aspect I would like to include.
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Heather:
Connectivism does not always equate to inclusivity. There is a plethora of digital content on the Internet that students can connect to for learning, but not all of it is culturally or internationally relevant to the diverse backgrounds of students. I have written a few articles to highlight the need for more inclusivity in our content that we provide to culturally and internationally diverse students. I hope these would be helpful.
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Our patient complaining of anxiety preoperative, we will start new project to prevent this complaint.
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Hello Hani,
This is an interesting area that the nurses at the Surgical unit discussed in their Nursing Journal Club months ago. They've discussed the same review article that Abdulqadir attached for you.
They were thinking to conduct an Evidence-based project to look for literature to allievate pre-surgical stresses. Interestingly, the issue raised after observing high blood pressure readings and taccycardia the night before surgey.
There is many feasable interventions that can be done such as (1) pre-operative structured visits the night before the surgery; (2)  Patients' round to Operation theatre before surgey. The latest might be argumentative, however there might be a turn around in bringing the theatre to them :) such as providing a friendly-booklet with real pictures and discription of the operation theatre environment.
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Specifically on  CBT for anxiety disorders
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Awesome !! Thank you so much for the great help :)
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Looking for the origin of the word anxiety in Spanish language
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Thank you very much for the useful information. It is so kind of you. Best wishes and thanks again
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I'm seeking for any reserches or studies on correlation between parents' couple's relation and anxiety disorders in their sons...
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I haven't come across any research articles on this specific topic. I appreciated your articles, Beatrice.
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I have found many papers that use the State-Trait Anxiety Inventory (STAI) trait part of the questionnaire to divide participants into low and high anxiety groups.
However, I want a scoring criteria to exclude participants with very low STAI trait anxiety and include all other participants (i.e., those with medium to high anxiety). The participants will not be clinical though but healthy populations.
Can anyone recommend papers that report the 25th or lower percentile of participants that score low on the STAI trait measure?
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Like Daniel, I am curious about using a cut score.  The continuous score generally offers information that may be more meaningful. 
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There seems to be quite a bit of short-term research, but I wonder if anyone out there is doing long-term research – 20-year or 10-year incidence of serious psychiatric disorders.
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Béatrice – thank you very much for your help. My malaria maven down the corridor is interested in conducting some research into this, and my own interest is in the potential role of mefloquine in triggering a psychotic episode in vulnerable people – probably teens and early twenties – similar to the effect of cannabis. It's a tricky design, because the exposed group will have travelled abroad, making selection of controls an issue.
Lars - good to hear from you! I hope all is well.
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In all my experiments, there is a fraction of stressed mice which when analysed using the dark/light transition test, prefer to just sit in the light and do nothing. They don't appear to explore the area, just to sit in one place and look around. Am i doing something wrong, or this is just a deeper form of anxiety disorder? did anyone come across such behavior?
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Based on my experience working with the Elevated Plus Maze, less anxious or stressed rats tend to spend more time in the open/bright arm of the maze, but will spend more time in the dark arm as a result of anxiety or stress. However, contamination may easily influence experiments such as this. If you test a couple of rats using the same equipment without cleaning between sessions, they may just stay around where the previous mice stayed regardless if they are stressed or not, because they feel comfortable.
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Greeting!
Could you please suggest any additional expected predictor of suicide among hospitalized psychiatric patients to be investigated for a future research?
This is the initial list:
1- being young,
2- male gender.
3- high level of education.
4- history of prior suicide attempts.
5- presence of depressive symptoms.
6- presence of active psychotic symptoms.
7- good insight to illness
Kind regards,,,
Ahmad.
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From my experiences doing epidemiological research studies in different countries (Japan and US),  the predictors are culture dependent.  Because each culture/country has different tendencies in terms of frequencies across age groups, gender differences, reasons for attempt, method of attempt, religious affiliations etc.  I'd be careful to generalize findings from other cultures.  Good luck with your research!
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Does anyone know of empirical evidence demonstrating the observation that distraction can modulate both reappraisal and rumination (indirectly through reducing distress) in the context of emotion regulation? This relationship is suggested in Susan Nolen-Hoeksema's review on rumination entitled "Rethinking Rumination" (2008, p. 410). This relationship is stated via the diagram on page 410, however no direct citations are stated indicating the empirical support for this claim. Based on the way it is phrased however, it seems that this question was addressed in work by Susan Nolen-Hoeksema and her colleagues - however I am having trouble finding this empirical support.
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There is a recent opinion paper on this topic, which includes some updated citation you may find interesting:
Also there are a few imaging papers trying to compare distraction and other emotion regulation strategies:
Kanske, P. Heissler, J. Schönfelder, S. & Wessa, M. (2012). Neural correlates of emotion regulation deficits in remitted depression: The influence of regulation strategy, habitual regulation use, and emotional valence. Neuroimage, 61, 686-93.
Schönfelder, S., Kanske, P., Heissler, J. & Wessa, M. (2014). Time course of emotion-related responding during distraction and reappraisal. Social Cognitive and Affective Neuroscience, 9(9), 1310-1319.
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Is there any evidence or personal clinical experience regarding the efficacy of antidepressants for depressive disorder and anxiety disorder in patients with carbon monoxide intoxication?
When a patient has previous history of depressive disorder and generalized anxiety disorder and later attempted suicide with subsequent carbon monoxide intoxication, is there any literature discussing the efficacy of antidepressants before or after the intoxication? Would the original antidepressant before the intoxication still be the best choice?
Would CO intoxication-induded Parkinsonism of the patient influence the choice of antidepressant?
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Once I had a patient who attempted suicide with carbon monoxide. She was with her baby, as how could the baby survive without her? She lived and was charged with homocide. I helped to get her hospitalized and eventually she was monitored as a psychiatric out-patient. This and other cases are discussed in my book, "Transforming Depression : Healing the Soul through Creativity." The 3rd edition (2002) is the most up to date. 
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I'm interested in studying medical school students' study habits and the ways in which they impact anxiety and depression.
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Jill, you look at papers by the following authors:
Sirin, E. F. (2011). Academic procrastination among undergraduates attending school of physical education and sports: Role of general procrastination, academic motivation and academic self-efficacy. Educational Research and Reviews, 6 (5), 447-455
Steel, P. (2010). Arousal, avoidant and decisional procrastinators: Do they exist? Personality and Individual Differences, 48, 926-934.
Steel, P. (2007). The nature of procrastination: A meta-analytic and theoretical review of quintessential self-regulatory failure. Psychological Bulletin, 133, 65-94.
Wolters, C. A., Pintrich, P. R., & Karabenick, S. A. (2005). Assessing academic self-regulated learning. In KA Moore, LH Lippman (Eds). What do children need to flourish? (pp. 251-270). New York: Springer.
van Eerde, W. (2003). A meta-analytically derived nomological network of procrastination. Personality and Individual Differences, 35, 1401-1418.
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I need this measure for my dissertation study.  I am also looking for a Spanish translated version. Thanks 
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email: 
they have used the BSI-21
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We are studing 5-6 age preschool childern for identifing anxiety disorders. We use spence childern anxiety scale paren form but we have observed that high scores in this tool didn't mean the presence of any anxiety disorders. In more case, high scores haven't related to pathology. Can anyone has ideas for guiding us?.
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Dear Omid,
I am not sure about using any scale for anxiety on that young children. All scales are validated for children 7 and more years old!
Personally, I do not believe that any other anxiety disorder can start at this age except specific phobia....and this also can be developmental characteristic. However, I am very interested in seeing your results!
Dejan
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CISD and CISM have been around since the early 1990s, but to my knowledge there have not been any valid and reliable tools to measure the effect or outcome of these interventions.
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Hello and although this does not directly address the question, I suggest that reading the Cochrane Collaboration review on this might be helpful to you (it provides a systematic review of the literature).  Psychological Debriefing for Preventing PTSD (Rose, Bisson and Wessely). I am a co-author.
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I'm trying to use restraint as a stressor to cause anxiety-like behavior in rats. The effect seems fine, OT% is about 14- 17%. However, the control rats seems unnormal, with only 19% of the time spent in open arms. I read from other literature that the control group usually reaches 25-30%. I'm wondering  that there are several innately extremely anxious rats in my control group. So can I pre-test the anxiety level of rats(using elevated-plus maze) to make a balance? But I'm afraid the first experience of EPM would affect the second trial. Has anyone else met the same problem like this? Thank you!
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Using the same test twice can dramatically affect performance on the second test.  I agree that using an alternate test of anxiety would help- you could do open field, and look at center time/surround time, light-dark box, or defensive burying.
However, that won't solve your problem of high baseline levels of anxiety.  It could have to do with rat strain, level of food deprivation, time of day for testing, sex or age of the rats, or level of lighting.  Here's just one example of a paper that demonstrates how some of these things can affect performance on the EPM- there are many out there.
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I am looking for a measure which can be used to assess the proposed criteria. If the measure has been published, any links to those papers would be greatly appreciated. Thanks!
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Hi Steven,
Hope this article useful
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The pt. is refusing all the psychiatric interventions and refusing to eat. However, receiving IV fluids and dextrose sporadically. 
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I have always reasoned that a patient who elects not to communicate is for the physicians' purposes in the same position as a patient who cannot communicate.  His wishes are not communicated.  In this sense, failure to exercise a capacity is the same as lacking capacity.  Dr. Breen's reasoning is similar. 
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In the document entitled "Highlights of changes from DSM-IV-TR to DSM-5" it says for social anxiety disorder
"A more significant change is that the “generalized” specifier has been deleted and replaced with a “performance only” specifier. The DSM-IV generalized specifier was problematic in that “fears include most social situations” was difficult to operationalize. Individuals who fear only performance situations (i.e., speakingor performing in front of an audience) appear to represent a distinct subset of social anxiety disorder in terms of etiology, age at onset, physiological response, and treatment response."
First, does anyone know what makes these individuals a "distict subset of SAD" especially in terms of physiological response.
Second, does anyone know the empirical evidence that supports this distinction (especially for physiological response)?
Third, does "physiological response" refer to self-perceived bodily sensations and/or actual physiological parameters (central/peripheral)?
Thanks!
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I only attempt an answer to your first question: Social anxiety disorder is strongly based on unrealistic expectations about other people's faultfinding interest in your performance of even trivial tasks like pouring out a cup of coffee ("do they see that my hand is shaking? What will they think of me when they see my hand is shaking? etc.). It testifies of a strong uncertainty about oneself, probably fostered by a learning history with much criticism and rejection by one's parents or one's peer group. In public speaking the expectations of a critical audience and of the impact of making mistakes are much more realistic. And the risk of making mistakes is much greater, just because one's performance is under pressure. The task is not trivial and it needs much training to become skilled in it.
Whether there is a physiological difference between the reactions of a social phobic and a person who fears public speaking seems to me of subordinate interest.
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Mindfulness is now widely accepted practice for improving physical and psychological well-being. Recently, one participant in mindfulness-based interventions who is trying to integrate mindfulness in every-day life experiences reported to me that she had experienced palpitation and headache during her mindfulness practice. This rare observation leads me to ask about the risks (negative consequences) of mindfulness practice!  
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Hi Ahmad,
When the body and mind enter stillness, what is already there - experiences held in  mind memory and tissue-held memory in the body, may emerge.  In my studies and practices in bodywork, energy work, mindfulness/meditation, yoga, etc., there has always been reference to these possibilities and recommendations to seek professional medical assistance, i.e. counseling services to work through what may bubble up.  The consequences you are contemplating are really a person's baggage unpacking, and that movement is a path toward wholeness. At the same time, special attention is prudent because a flood is not so healthy rather a gentle peeling of the layers as the person is ready.  In short, it's not so much the methods that pose risk (in my opinion) but the resistance to acknowledge what's there, the readiness/committment to "do the work", and the willingness to seek appropriate services  which may include a variety of providers, strategies, and most importantly, timing. Your thoughts?
Best,
Victoria
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Looking for a seminar speaker on computer anxiety as applied to healthcare. Hoping I could have at least an hour of their time online for a webinar within the next month of May.
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Dear Francis,
Thank you for the invitation, and I look forward to presenting the webinar on computer anxiety in healthcare professionals to your group at the University of the Philippines, Manila.
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Chronic stress can lead to anxiety in some people, while it can lead to depression in others. Some people with chronic stress may experience both anxiety and depression. It seems not clear how stress, anxiety, and depression contribute to each other. How can we interpret these different combinations of co-morbidity?
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Very interesting discussion. It's interesting that the literature really does not try to parse out when stressors lead to either depression or anxiety, as they are highly comorbid with each other, and they overlap with multiple symptoms. Even their treatments with CBT and antidepressants are similar, and making determinations if this is anxiety or depression really does not matter much, as it does not inform further clinical treatments. In my clinical experience, stressors are either handled via adaptive coping skills, or they aren't via maladaptive ones. These patients may then start having adjustment problems, and you notice the specifiers for adjustment disorder includes -with anxiety, -with depressed mood, and -with anxiety and depressed mood. If the stressors continue, then either a depressive disorder or an anxiety disorder emerges, and this tends to go back to CBT theory about thoughts and appraisals about the fearful stimuli and stressors, and this seems to be a significant variable which in turn determines which disorder emerges.
It also appears that anxiety and depression share the same neurobiology: it comes down to the interaction of genetic vulnerabilities (family history) with environmental influences (major life stressors), and it is this interaction which leads to abnormal processing circuits in the brain (hyperactivity of the amygdala to fearful stimuli and stressors). This hypothesis has been supported by a recent study which revealed that people with increased reactivity of their amygdala to fearful stimuli (as measured on fMRI), when they also experience a major life stressor, are more at risk to developing either anxiety or depression up to 4 years into the future: http://www.ncbi.nlm.nih.gov/pubmed/25654256. Further research should examine how the differentiation is made between the development into depression or anxiety, following study subjects with high amygdala reactivity to fearful stimuli who have also endured a major life stressor. I hypothesize that it is the thoughts and appraisals of the stressors which differentiates anxiety from depression, as discussed previously by other researchers who have replied to this interesting thread.
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Signs and symptoms of depression in mothers of children with autism are frequently reported. However, based on extensive clinical observations and self reported data, I constantly observed that these mothers report specific depressive symptoms more than others. I did not observe this phenomenon in patients with schizophrenia or bipolar disorders. Is there any evidence supports this??? or it is a merely chance?  
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I'd like to join others in saying "Yes" to your question, Ahmad.
Indeed depression is a universal phenomenon and there are subtypes of depression. However, from the perspective of multicultural psychotherapy and international/global psychology, there are differences in one’s symptom manifestations, cultural explanations, and impact of depression on oneself and one’s intimates, depending on one’s cultural identification, acculturation to the Western cultural worldviews, and diverse backgrounds (Falicov, 2014; McGoldrick et al., 2005; Sue & Sue, 2013).
In terms of treatment, there are also differences in one's expectations of the treatment goals, processes and relationship with the healer (Cheung, 2009; Hong & Ham, 2001).
DSM-5 has provided an excellent outline for cultural formulation (OCF) and Cultural Formulation Interview (CFI).
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From my clinical experience it seems that while some panic attacks symptoms can be quite overt and easily noticed (like sweating, pallor, shaking) these may also be mis-attributed by observers and many less obvious symptoms may not even be noticed.  I'm wondering if anyone is aware of published research that has attempted to measure how effectively observers can gauge levels of anxiety and panic in someone just by watching them perform a task?
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Hi Kelly,
I did work on panic attacks many years ago. I recall that often times the person who is having the attack can not talk because his or her throat is so dry. This seemed to be overlooked in the literature at that time.
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Anxiety sensitivity is a temperamental factor in explaining of emotional disorders. it had been studied in many researches, but can high scores in tools of assessing this factor predict treatment output in CBT?
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Dear Omid, 
Cogn Behav Ther. 2006;35(4):248-56.
A brief cognitive-behavioral approach to reducing anxiety sensitivity decreases pain-related anxiety.
Watt MC, Stewart SH, Lefaivre MJ, Uman LS.
 
Abstract
Anxiety sensitivity (AS; fear of anxiety-related sensations) is a known risk factor for anxiety disorders and recently has been linked to pain disorders. The present study was guided by the hypothesis that a program designed to reduce AS levels might also result in a decrease in anxiety related to pain sensations. Female undergraduates, selected as either high or low in AS according to screening scores on the Anxiety Sensitivity Index (ASI), were randomly assigned to participate in 3 1-hour, small group sessions of either cognitive behavioral therapy (CBT; psycho-education, cognitive restructuring, and interoceptive exposure) or a non-specific treatment (NST). Immediately prior to and following the intervention, participants completed the 20-item Pain Anxiety Symptoms Scale (PASS-20). Consistent with hypothesis, results revealed a 3-way interaction between AS group, intervention condition, and time on PASS-20 total scores. Only participants with high pre-morbid levels of AS assigned to the CBT condition showed a significant reduction in scores on the PASS-20 from pre- to post-treatment. Implications for improving CBT approaches for pain disorders are discussed.