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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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We can connect you with fellow researchers. We provide fair pay and recognition for supporting your peers.
Become a Peerwith expert
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I appreciate this great effort, and I hope to join you, but it is possible to know a biography of the work, as well as your presentation of a comprehensive plan on the most important achievements and humanitarian psychological works that serve patients or those who need them, because as you know, we have a duty towards the right of every patient. Therefore, we are obligated to offer our sincerity to work before God Almighty, and before those who need guidance and psychological treatment.
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As often in medicine animals are ( SADLY) used in experiments .A new study of mice shows there are important links between human and mouse minds in how they function -- and malfunction. Researchers at Washington University School of Medicine in St. Louis devised a rigorous approach to study how hallucinations are produced in the brain, providing a promising entry point to the development of much-needed new therapies for schizophrenia.
The study that was published in the journal Science, lays out a way to probe the biological roots of a defining symptom of psychosis: hallucinations. The researchers trained people and mice to complete a computer-based task that induced them to hear imaginary sounds. By analyzing performance of the task, the researchers were able to objectively measure hallucination-like events in people and mice.
This approach allowed them to study the neural circuits underlying hallucinations, potentially fully opening up the study of mental illness to the kind of scientific studies that have been fruitful for diseases of other parts of the body. My concern is that despite the positives and even if there are similarities, can a study like this be of great value when it comes to humans who has a fundamentally different cognitive ability and brain structure? I agree that we can see tendencies and the study gives an insight, however can this ever fully be transferred to humans? also see other risks as well as grave ethical concerns that applies with all experiments on animals. What are your thoughts?
Best wishes
Henrik
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The comparative study of living organisms is standard laboratory practice, e.g. the knowledge transfer of animal experiments to humans. Concerning psychiatry, this may be the human medicine par excellence, and I personally (and methodically) doubt that, in this case, the results of veterinary medicine can be applied to humans successfully.
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Prudent prescribing of antimicrobial drugs to hospital inpatients may reduce the incidence of antimicrobial drug resistance and healthcare-associated infection. Despite strenuous efforts to control antimicrobial drug use and promote optimal prescribing, practitioners continue to prescribe excessively; it is estimated that up to 50% of antimicrobial drug use in hospitals is inappropriate. Antibiotics have several drug-drug interactions (DDIs) with psychotropic drugs (mainly antidepressants, antiepileptics, antipsychotics), which can lead to adverse events, treatment failure and significantly rise the costs of treatment. 
Currently, very little is known about antibiotic prescribing patterns in psychiatric hospitals, including the frequency of potential DDIs between antibiotics and psychotropic drugs.
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Regardless if you have a psychiatric diagnosis and not, you can have infections and other p0hysical disorders. My experience is that too little focus is put on these patients' physical disorders. In the early years alcohol and penicillin was recommended not to be taken together. This was not due to any interaction between alcohol and penicillin but it was a precaution that sailors and others with sexually transmitted disorders could forget to take their antibiotics when drunk.
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I performed a moderation test and I found a significant moderation effect. The post hoc tests showed that both +1SD and -1SD lines are significant. How can I interpret this? Is it correct to assume that any levels of the moderator can increase (in my case) the relationship between x and z? Can I assume a moderating effect for the variable that was entered as a moderator?
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Can I ask how to apply post hoc test on the moderation test?
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Are there good evidences that support the role of vitB12 in schizophrenia? 
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I have been diagnosed and medicated over twenty years with a psychiatric condition that medication works well for me.
I was on 100 mg of Seroquel for a long time with no problems, then had to be hospitalized.  The Dr. told me it wasn't a therapeutic dose, even though it had been working just fine for years.  He raised my dose to 300 mg.  When I went home I felt like I would die every time I went to sleep went back to the hospital then the same Dr. gave me Geodon, which did not even work at all and then I was threatened if I did not take an injection to go to court.  They messed my medication up, not me.
I understand the holistic approach, but requiring services the client does not want, does not benefit the client in any way other than someone to talk to.  I don't think Social Workers should be making diagnostic decisions anyway.  It is a waste of time and money and Paternalistic.
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The assumption is that the "social worker" or "therapist" or "counselor" (all of whom do not prescribe medication) can discern from the conversation signs of intellectual and emotional impairment. If you are just having challenges and difficulties in life that cause you discomfort then medication is not called for. If you are unable to deal with challenges due to mental or emotional impairment then you may need medication (or medication change). To save the medical doctor (psychiatrist) time the client is "screened" with this approach. It is to use the doctor (who is usually more expensive) only after it has been determined what your problem is (physiological or not physiological). A third option is to seek out practitioners who understand the emerging orthomolecular techniques that address the dysfunctional metabolic cycles that underlie various mental illnesses. This is more problematic if you have been on medication for 10 years or more but it may be worth consideration. I review a popular book "Nutrient Power" written for the non-expert on this approach that I think has great promise and quality researchers involved at:
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Will you consider symptoms of (hypo-)mania (e.g. HCL-32(33R) in your research on sudden cardiac death?
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How?
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I have not found many studies about this treatment. It has been approved by FDA based on very preliminary evidence. How much time does FDA take in general to approve a treatment in mental health field?
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I agree that we do not know how eTNS works on ADHD children, but in terms of clinical application, I recommend to use it because there are parents worrying about side effects of medication as well as being unable to manage ADHD symptoms.
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I just came across a really interesting point of view in a clinical manual by a leading author in clinical treatment in Spain, Miguel Ángel Vallejo. He claims, based on a study by Rude and Rehm (1991)*, that psychotherapy is most effective when it boosts already-existing capacities and skills, rather than when it focuses on ameliorating deficits. That seems to run counter to much of what I have seen before in psychotherapy; does this idea match your clinical experience, or do you have any additional bibliography that might support this claim Thanks a lot!
*The citation to this article is given as "Rude, S. S., & Rehm, L. P. (1990). Cognitive and behavioral predictors of response to treatments for depression. Clinical Psychology Review, 11, 493–514"; however, all I can find online is this other article, with a different name, although (apparently) similar content: https://psycnet.apa.org/record/1992-06180-001
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"In psychotherapy, is it better to boost current skills or mitigate deficits?"
I just discovered this important question. If we go beyond the question of depression alone and ask a more general question about the psychotherapies - from psychoanalytic to behavioral and cognitive therapies to relational therapies, we can discern more general patterns of what happens in therapy.
Using information theory and systemic therapy as a model (but this applies to all therapies), we do three simple things in therapy (Di Nicola, 1997):
  • Enhance uncertainty (show that their current repertoire is limited or that their way of framing things can be improved)
  • Introduce novelty (suggest other ways of examining the problem from new perspectives)
  • Encourage diversity (stimulate new ways of thinking and being, beyond their current repertoire in order to be more adaptive to current and future challenges)
So, my specific answer to this question - "In psychotherapy, is it better to boost current skills or mitigate deficits?" - is that another option is missing which is to introduce novelty, new ways of looking at things and new ways of living. This means in the frame of this question, new skills, as opposed to boosting skills already in place or mitigating lack. Let me be clear: offering to model or teach new skills is not necessarily addressing a lack. It may simply be the case that the person never confronted a given situation and needs to add to their repertoire of skills.
Vincenzo Di Nicola, MPhil, MD, PhD
Université de Montréal &
The George Washington University
Reference: Di Nicola, V. (1997). A Stranger in the Family: Culture, Families, and Therapy. New York & London: WW Norton & Co.
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The symptoms described by Freud were : episodic episodes of "psychosomatic" dyspnea, cough, afonia (without a medical explanation and then " conversion" symptoms ) but also : depression, " hysterical "
social withdrawal, and "taedium vitae" ( i.e. for the modern " emptiness" ? )
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No - in that the history of Borderline/Borderland (WA White 1912) shows it to be a " diagnostic waste bucket" for persons unaware of E Minkowski's work on structure (1924). Conversion points to hysteria - no more but no less.
David F Allen
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Is that ok with using high-risk suicide in MINI (mini international neuropsychiatric interview) as outcome in major depressive disorder ?
If no, is there any  clear or general definition for the outcome of high-risk suicide in major depressive disorder ? Such as suicide attempt ?
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I suggest suicidal ideation, I attach our paper:
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Why do you think such links exist?
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Psychology is the result of close observation of many individuals at various mental states, usually those who have a disease or a condition. Hence it can be faulty, though most of the times, it is not. Since each human has some disease in him/her. True religion is close observation of the individual self itself and then progressing above by self cleansing through sadhana/meditation. Book religion is true only for those with open eyes, else it is a poison, coz 'the reading I' becomes the character of the book read
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Cycloserine is an antibiotic used to treat tuberculosis. It has several side-effects, including irritability and anxiety. It is an analogue of D-alanine. It has been used as an anti-depressant, based on its effect on NMDA receptors.
I am being asked to provide psychiatric support to a patient who is facing 8 months of treatment with cycloserine, and wonder if someone has experience of psychopharmacological interventions that might reduce the negative effects of the cycloserine?
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If Cycloserine can't be stopped and the depressive symptoms are severe I would recommend a psychofarmacologic treatment. The novel antidepressant vortioxetine could represent a good option as It helps depressive and anxiety symptoms and has no farmacologic interactions
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As part of our investigations into the current state of psychiatry, I would like to ask how academics and practitioners, researchers and clinicians, and of course professors of psychiatry, see contemporary psychiatry and its future. My colleague Drozdstoj Stoyanov, MD, PhD, and I are writing a book called "Psychiatry in Crisis" (see Research Project on "Psychiatry in Crisis") in which we pose and will try to answer the following question:
Is psychiatry a social science (like psychology or anthropology), is it better understood as part of the humanities (like philosophy, history and linguistics), or is the future of psychiatry best assured as a branch of medicine (privileging genetics and neuroscience)?
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What are the practical implications of classifying Psychiatry into one of the mentioned categories? Would doing so necessarily bring Psychiatry out of the "crisis' mentioned (is it really in a crisis?). My own Psychiatry colleagues used insights from all the disciplines mentioned. For example, several were involved with the issue of euthanasia and the ethical issues involved (philosophy), issues of anthropology were involved (do forms of mental illness manifest themselves differently in different cultures), and neurology and neuro-psychology (are there underlying specific correlations with present diagnostic categories?). An additional issue is that the boundaries between the disciplines mentioned are not fixed. Further, some areas of medicine have changed to be concerned with enhancing human beings rather than just fixing organic problems, will Psychiatry follow this path in the future? I've probably just muddied the water, but I'm not sure why the question needs to be asked.
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This is on APA Psychnet for purchase. However, I don't think it is the actual questionnaire.  Any help appreciated.  Thanks.
Salovey, P., Mayer, J. D., Goldman, S. L., Turvey, C., & Palfai, T. P. (1995). Emotional attention, clarity, and repair: Exploring emotional intelligence using the Trait Meta-Mood Scale. In J. W. Pennebaker (Ed.), Emotion, disclosure, & health (pp. 125-154).
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Thank you
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What are the problems for a patient diagnosed with schizophrenia with CVD and metabolic syndrome on beta blocker atenolol 
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Atenolol is a beta-blocker with suboptimal pharmacodynamics and suboptimal 24-hours BP lowering coverage. 
It decreases vasodilation in the skeletal muscle and, presumably because of this, impairs glucose tolerance. Its administration is associated with increased incidence of diabetes. 
As other drugs in this class, it has several and severe side effects such as depression, fatigue, impotence, impaired peripheral circulation (cold extremities) ...
For me and many other experts, this drug is out for the treatment of hypertension. If you still would prescribe a beta-blocker in hypertension as a 3d or 4th add-on drug, I would definitely go to a vasodilating beta-blocker such as carvedilol or nebivolol. These drugs has no definite effect on glucose intolerance. 
Hope this answer is contributive. Please let it know. 
Best regards,
Thierry
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Is it in the best interest of the patients , not to highlight certain side effects of medications or procedures which might have a Nocebo response?
For example: Do we highlight to a  man that beta blockers can cause impotence before starting beta-blocker??.
More patients are having negative responses to various medical interventions when they are told more than they should know about the treatment.
Are we here to in this profession to help patients benefit from the treatment modalities or are we here to do the job and safeguard our self without having to worry about what happens to the patient? 
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We should warn about the ADR but also tell the percentage of people who might develop it in a layman language. We must safeguard ourselves first. In developing countries, doctors are getting abused physically almost every day.
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In real clinical practice some patients are treated with combination of clozapine and another depot antipsychotic. Although we have a positive evidence of clozapine combination with some antipsychotics, clozapine should not be combined with depot antipsychotics, because of several adverse events, which can not be discontinued very easy in patients treated with depot. In clinical practice we often have problem that we have positive symptoms (residual) with only clozapine and therefore combinations could be used. In my point of view many combinations should be used first (e.g. combination with lamotrigine, combination with another antipsychotic non-depot, combination with N-acetylcysteine) before this potentially risky combination.
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Before combining with other antipsychotics, it might be helpful to control serum levels, because particularly in clozapine, non-compliance or only partial compliance is a frequent cause of treatment resistance.
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Must we change their anti-epileptic treatment before ECT ? 
Any risk of dangerous sides effects like status epilepticus ?
Must we adapt the protocole of ECT ?
Have you clinical experience about that or any evidence based ?
Thank you
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Electroconvulsive therapy is safe and effective in patients with depression and comorbid epilepsy.  I noticed no difference in remission rates or side-effect rates in my patients who also had seizure disorders.  An additional benefit is that seizure threshold rises during ECT as a consequence of the treatments.  It is quite ordinary during a course of ECT treatments to see increased refractoriness to seizures, reflecting the increase in seizure threshold.  It is dealt with by simply increasing the stimulus dose.  Done correctly, ECT is a safe and appropriate treatment for depressed patients with epilepsy.
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You wrote in the abstract of your article (Overreactivity of the psyche or the soma? Interindividual associations between psychosomatic symptoms, anxiety, heart rate, and end-tidal partial carbon dioxide pressure. Psychosomatic Medicine 56(6):533-40.) “The findings suggest that reports of psychosomatic symptoms represent two distinct components: one that is primarily psychological (and is unrelated to physiological factors) and a second that reflects objective variance in physiological functioning. The influence of the first component is probably greater than that of the second.”
My answer:  We can prove that physiological events (after chronic hyperventilation) are the causes of the psychosomatic symptoms and psychological factors are only their consequences.
We discussed the topic: how we think that chronic hyperventilation (and its metabolic compensation) can cause "physiological panic attack," which may be intensified by the fear of attacks. (A quotation from Sikter A, Faludi G, Rihmer Z.: The role of carbon dioxide (and intracellular pH) in the pathomechanism of several mental disorders. Are the diseases of civilization caused by learnt behaviour, not the stress itself? Neuropsychopharmacol Hung. 2009;11:161-73.)
“We made an attempt to integrate the three main theories (Sikter et al., 2007b. See attached the full text article: Sikter A et al.: The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder.  Rev Bras Psiquiatr. 2007; 29:375-9.) about the relationship between hyperventilation and panic disorder, even though according to Wilhelm et al. (2001a), these theories would include antagonistic contradictions. The three statements are: A/ hyperventilation is a protective/preventive mechanism against panic attacks; B/ it is a physiological response to hypercapnia; C/ it can induce panic attacks. We think that panic attack is a cascade of events where hyperventilation has different roles in different times. Chronic hyperventilation is probably a precondition of (respiratory subtype) panic attack, although it defends against panic. While it exsists, spontaneous panic attacks cannot arise (see statement A). Chronic hyperventilation can be generated by either organic diseases (e.g. asthma bronchiale) or mental conditions (e.g. sighing or crying for a tragedy). Compensational mechanisms set off metabolic acidosis that neurtralizes hyperventilational alkalosis, this compensational process lasts at least for a week. In the state of compensated hypocapnic alkalosis extra- and intracellular pH stays in the normal range. The depressed pCO2 level starts to go up to the normal level (or slightly higher) before the attack. The elevating carbon dioxide promptly diffuses into cells and causes acidosis, which increases catecholamine release from different cells (e.g. noradrenaline release from locus coeruleus) (Filosa et al.). On the other hand, elevating carbon dioxide level also evokes acute hyperventilation (through a brainstem reflex), which may be more vigorous than previously. (see statement B). At this point hypercatecholaminemia (induced by previous acidosis) and alkalosis (abruptly decreasing pCO level) evolve at the same time. Alkalosis multiplies CNS-responsiveness to catecholamine levels, and it lasts for several minutes to break down catecholemines. This coexistence means an intense sympathicotonia, a very high arousal. (The cascade of events is similar to Steen’s animal model – a hypercapnic period is followed by a hypocapnic one) (Steen et al.). High catecholamine level/sympathicotonia can provoke panic attacks (Cameron et al.). Panic attack is precipitated by this second (acute) hypocapnia (see statement C) plus catecholaminemia induced by previous acidosis. We have illustrated panic attack on a theoretical diagram. According to this panic theory intra- and extracellular pH is thoroughly compensated before the attack, but the acidosis would be overcompensated by acute hypocapnic alkalosis during the attack. The main problem is that the different compensational mechanisms work out at different rates. Carbon dioxide level can change in the whole organism in a few seconds, the elimination of catecholamines lasts for several minutes, and the clearing of blood from metabolic (“titratable”) acidity takes at least one week. This is one of the many reasons there is no perfect compensational mechanism.”
Physiological events of the respiratory type of panic attack (a hypothetical model) See the attached figure (jpg)
·         Period A/ Chronic hypocapnic alkalosis is compensated by chronic metabolic acidosis (pH is in the normal range). The arousal is normal.
·         Period B/ The pCO2 level starts to normalize (is elevating): intracellular acidosis arises, catecholamine output increases. The arousal is normal or decreased.
·         Period C/ The pCO2 level reflexively decreases, the responsibility of neurons to the catecholamine levels increases AND the catecholamine level is still high – a panic attack can arise
·         Period D/ Feeling and fearing of somatic sensation  elevates catecholamine level and decreases pCO2 level
The periods A/, B/, and C/ are single physiologic events. Only the period D/ is a psychic phenomenon. Without chronic hypocapnia, there is no respiratory panic attack. If the breathing results in eucapnia and it is regular, there are no hyperarousal, anxiety, and somatic sensations (e.g. GAD)- or they exist only on a minimal level.
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Dear Colleagues, Dear Dr. Chandradasa,
The "psychological activities without physiological alterations" do not exist. Psychological activities are carried out by neurons. Neurons work through physiological mechanisms. Membrane potential, action potential, active and passive ion transports, intracellular ion patterns, intracellular pH, hormone receptors of the membrane, etc. are physiological factors - a neuron does not work without them. If physiological parameters are normal, the neuron will work normally. If the physiological parameters are abnormal, the neuron will work abnormally.
Dyspnea is not an imaginary symptom; there is intracellular acidosis mostly in its background. (Please refer to the graph I presented on the text. It depicts an example how does intracellular acidosis arise during PD.)
Andras Sikter MD    
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Reports of altered cation transport genes and their transmembrane protein transcripts in cultured cell lines from bipolar patients were judged as irreproducable by other research groups, and the original report was eventually withdrawn by Gershon and colleagues. In the 15-25 years since, have there been in vitro studies that either support or further debunk the theory that hereditary differences in Na+ Li+ countertransport levels in peripheral blood or cultured cell lines from patients might be useful surrogate markers for the clinical diagnosis of affective disorders or clues to their pathophysiology?
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A very interesting question. I know that a lot of work now around identification of biomarkers for bipolar disorder focus more around inflammatory cytokines; some of these studies reference Na-Li counter transport. You may be able to track down more recent research by searching for this type of inflammatory biomarker research as a backdoor to answering your question. Good luck!
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Seems that they have higher nocebo effect. Did you know researchs about most frequent nocebo signe and symptoms in panic disorder?
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Hi-- yes.  People with panic disorder are characterized by interoceptive hypersensitivity, specifically (a) an attentional bias toward signs of physical disturbance and (b) catastrophic misinterpretations of their physiological disturbance.  So they can be sensitive to anything that makes their bodies feel strange.
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In a very disturbing outcome last week, a young woman was found unconscious in her car on Staten Island in New York City. The responding police took her to the nearest ED (SIU Hospital) where the treating physician correctly diagnosed opioid overdose, and administered naloxone. The pt became conscious, and was discharged into police custody 6 hours after receiving IM naloxone and showing "healthy" vitals. She was incarcerated and died a few hours later in jail of an opioid overdose. My initial reaction was that 6 hours is not enough time to be certain that an opioid OD pt is stable and ready for discharge, but after reviewing the scant literature on the subject, I found articles like the one attached (NEJM) stating just that - administer naloxone, wait six hours, if oxygen sats and HR and BP are fine, then discharge. Of course, this presumes many things, predominantly that the pt has ODed on a short-half life opioid like diacetylmorphine (Heroin) and not a long-half-like one like methadone (which could explain the tragic consequences of last week). Conceivably, a pt could OD on a long-half-life opioid, be revived by naloxone, and then die of respiratory depression as bioavailability returned. Does anyone know of any newer (DOI: 10.1056/NEJMra1202561) and more nuanced protocols for the treatment of opioid ODs in the ED?
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Although I was not able to find any newer protocols for the treatment of overdoses in the emergency room, I have a few comments I would like to make about tragedies such as this and the linked guidelines.
First, while the flowchart in the NEJM article mentioned the consideration of discharge after 4-6 hours of observation (post naloxone infusion given the obtainment of normal vitals), the supplementary writing suggests that 12-24 hours of care are needed when a continuous naloxone infusion is administered. It is interesting, that both yourself, and the health professionals treating the deceased patient, both cited/exercised 6 hours of observation. While you noted the apparent inadequacy of this; the treating physicians deemed this acceptable. The treating physicians were most likely familiar with these guidelines which seems to suggest a very real danger of a paint-by-numbers approach to medicine. Instead of recognizing the caveat printed in the NEJM article, most individuals appear to simply focus on the algorithm presented.
Second, a few things about the events leading to the death of the patient. It is odd, that during the 6-hours of observation, the guidelines do not place a specific recommendation for the use of toxicology screening to identify the specific opioid or the presence of polysubstance use. Maybe the physicians who treated the deceased patient performed this screening, but this seems unlikely as people love to report on the atrocities caused by specific opioid agents. Also, I would like to know why this person was arrested and incarcerated. Unless she had some quantity of illicit drugs on her person, there doesn't seem to be cause for arrest. It is disgusting that law enforcement officers view drug users as criminals and circumvent reasonable thought in order to get a pat on the back from extreme teetotalers (unless of course there was a legitimate reason for arrest). Additionally, why was this woman allowed to die in the jail, did nobody check on a compromised inmate who was just released from the emergency room for a drug overdose as few hours ago? While respiratory depression (maybe?) was the means by which the patient/inmate died, the real cause of death appears to be negligence. 
Third, the most reprehensible thing in the passing of the unconscious female motorist, was her opioid overdose was extremely treatable (as evidenced by this person’s temporary recovery). This is the real tragedy of these deaths; they can be easily prevented. At this point, I need to rant on the ramifications of sensationalizing deaths resulting from opioids. Thanks to the superfluous war on drugs, people seem to views occurrences such as this as proof that these substances are a treacherous societal scourge. This is a major component in the push for physicians to avoid the use of opioids/opiates in treating patients. This is foolishness and other analgesics (NSAIDs, acetaminophen, etc.) are similarly dangerous (though possibly less fatal [Solomon et al., 2010]) and, therefore, do not make the choice of pain management any simpler.
Most of this content is somewhat irrelevant, but I just thought I would share my views on the failings of overdose management. I am glad to see that someone (you) recognized the insufficient guidelines in treating these occurrences.  
References: 
Solomon DH, Rassen JA, Glynn RJ, Lee J, Levin R, Schneeweiss S. The comparative sagety of analgesics in older adults with arthritis. Arch Intern Med. 2010;170(22):1968-1978.
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In my 35 y. long experience, real bipolar disease i.e. alternating phases of severe depression, normality and real mania is erroneoulsly extended to include banal fluctuations of unipolar endogenous depression. Do you agree ?
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I agree with you.
In case of Bipolar disorder I, the manic episodes are well established with definite symptoms and signs of manic episodes.
Whereas in case of Bipolar disorder II an elaborate history is needed from the patients and the family members to establish the hypomanic episodes  to differentiate them from the patient's very own personality.
If the disorder starts very early in life of the patient even before the basic personality of the patient  is established, then the diagnosis of bipolar disorder II  with the dubious diagnosis of an episode of hypomania  versus the patient's personality itself becomes difficult.
I think there is always a gray area when it comes to Bipolar II as compared to unipolar depressive disorder. 
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We have found within our community specialist PD team there are a small number of service users who present with exceptionally high risk clinical problems, complexity and comorbidity that they cannot be safely contained and supported in community settings. Their needs are complex, and often require more intensive and in-depth assessment, reformulation and stabilisation work which cannot be safely done within a community setting or whilst on an acute inpatient ward. Such service users, when in the stage of severe chaos, self-harm or suicidality may find an acute ward too stressful and over stimulating for them, which can lead to their attempts at coping to get worse, rather than better. The tendency to regress and lose skills and abilities whilst in an acute hospital setting has been well known clinically (e.g. Paris, 2004; Bateman and Krawitz, 2013).
Current research evidence and guidance on the use of hospital admission is mostly based on expert opinion and a little empirical research. Expert opinion and guidance suggest that admissions should be avoided as far as possible, but where needed, they should be used for acute crisis management rather than chronic risks and be as brief as possible (NICE, 2009; Paris, 2004; Krawitz and Watson, 2008; Fagin, 2004). There is some evidence that brief planned admissions are no more harmful than standard treatments (Van Kessel et al, 2002). 
We are considering the development of a specialist unit where these focussed admissions may occur safely in order to stabilise service users so they are more abel to engage in evidence-based treatments in community settings.
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Hi Stuart,
Maybe you are allready familiar with this paper but at least it shows some preliminary results suggesting that DBT might provide an effective treatment in Institutional settings.
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I am reviewing what was usual practice in the 1960's and 1970's.
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Thank you all for taking the time to respond.
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I am looking for research that supports (or refutes) the effectiveness of inpatient psychiatric hospitalization.
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Per APA guidelines and EBR, inpt hospitalization is not recommended, nor is it particularly effective, for those suffering from Borderline Personality Disorders. If it happens for reasons of safety it should be brief and followed up by a robust plan of Partial Hospitalization or outpt tx.
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I would regard D-K effect as Theory of Mind (ToM) deficit. It is less of narcissism and more not being able to compare one's low cognitive abilities with others' mind-set.  Certainly within psychiatric domain.There are also limitation in formal operational cognition that might fall outside typical psychiatric practice. 
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Hi, our research team wants to do a pilot-study on psilocybin. Does anyone have any idea on how we can buy this substance? Can anyone help us on international laws on doing these kind of research in Iran?
Previous published researches on psylocibin haven't mentioned how they provided this substance. unfortunately we don't have necessary facilities to synthesis pcylocibin on our own.
thank you in advance.
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Under the United Nations drugs conventions psilocin and psilocybin are controlled drugs, and the UN guidance is that national laws of member states should make these hallucinogenic substances illegal to possess or supply without a license for medical and scientific research. I do not know what the drug laws are in Iran, but in the UK scientists typically find it very difficult to get a Home Office license to conduct research with hallucinogens like those found in the psilocybe mushroom - which was totally banned, in fresh and dried forms, by the UK's 2005 Drugs Act, which made it a Class A and Schedule 1 drug. 
However, one interesting recent avenue involves a report that psilocybin has now been found in a lichen, when it had previously only been identified in psilocybe mushrooms. Depending on the law in Iran (and other countries), it might be more feasible to use lichen rather than fungi as a source of psilocybin - it is worth checking out: http://volteface.me/psychedelic-lichen/
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I am using the Positive and Negative Affect Schedule as the primary outcome within a trial.  I therefore need to stipulate what the MCID will be.  Does anyone know of a precedent for this or have any suggestions on how we could arrive at a figure?
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Thank you for this but I meant the PANAS (Positive and Negative Affect Scale) not the PANSS. 
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Hi,
I am looking for a scale to assess fatigue ("Müdigkeitssyndrom") in German. For example, a validated German version of the "Fatigue Assessment Instrument" (FAI) or the Chalder Fatigue Scale (CFL). We would like to assess fatigue in Hep C patients.
Danke!
Steffen
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Guten morgan. POMS validiert Deutsch. 
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I am trying to find a validated Falls assessment tool for our psychiatric patient population. The Johns Hopkins tool we currently use places all of our patients on falls due to medications that place them at risk.  I would like to use the Wilson-Sims Falls Risk Assessment tool. Does anyone use this tool? It appears to be validated in the literature. I'm trying to find out if it is free to use? 
Thanks
Cindy 
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Have you seen this? Handy comparisons:
PDF]Looking for a Psychiatric Fall Risk Assessment Tool - JSciMed Central
Feb 24, 2016 - a comparison of selected fall risk assessment tools are listed in a table. ... Wilson Sims Fall Risk Assessment Tool (WSFRAT) [14]. The latter.
This is the source of the assessment:
Validated Fall Risk Assessments | allnurses
allnurses.com › Nursing Specialties › Psychiatric Nursing
We have devoloped a psychchiatric fall risk assessment tool. The "WilsonSims" assessment tool. It is easy to use and we belive it was helpfull in cutting the fall ...
Regards
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Recently I learned of the potent CYP1A2 induction effects of proton-pump inhibitors (ie. omeprazole etc). These medications can significantly reduce olanzapine and clozapine concentrations. Which medications are we overlooking when it comes to CYP1A2 induction?
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Here are some drugs that induce CYP450 1A2: and that can reduce the AUC of olanzapine. The ratio of the AUC olanzapine alone and in the presence of these inductors(AUC*) is as follows :
1-Ritonavir (200-400mg/d) : AUC*/AUC = 0.89
2-Ritonavir (600-800 mg/d) : AUC*/AUC = 0.56
3-Darunavir: AUC*/AUC = 0.89
4-Lopinavir:AUC*/AUC = 0.84
5-Rifampicine (450-600 mg/d): AUC*/AUC = 0.66
6-and also Tobacco (10-20/d ) is an inducer of CYP 450 1A : AUC*/AUC = 0.78
NB: in the absence of an inducer the ratio is equal to 1.
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Papakostas et al showed adjunctive LMF to be effective in treatment of mdd in 2012 with a NNT of 6 patients. The 2014 follow up article in J Clin Psych by Papakostas et al assessed biomarkers of LMF responders showing no statistically significant difference in HDRS-28 scores between MTHFR 677 CC (wild type) and MTHFR 677 TT (varient, reduced activity) patients.
Reduced or inactive MTHFR activity is not specific to depressive disorders.
Where does this leave us when depressed patients present with reduced or inactive MTHFR? I am thinking it should not lead towards LMF supplementation.
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Agree with Ian Mcgrane. This is a new market, with Deplin claiming to be superior to Enlyte and visa versa: the representatives are doing their job well, as are the new companies that tout the benefits of MTHR genotyping.  BUT THE SCIENCE IS NOT THERE TO JUSTIFY MAKING THIS STANDARD CLINICAL PRACTICE. And we should not be wasting patient's $ on this without basic and translational research making risks vs benefits clear.
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Just as uncertain that I am about the interest of this perspective in the scientific World I am just as convinced about it gains if conducted.
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If you let go of the interview method, you could focus on the history of the issue of mental competence, which mostly used in forensic psychiatry, but would shed light on your question. See for example the book by Daniel Robinson Wild Beasts and Idle Humours The Insanity Defense from Antiquity to the Present (Harvard University Press, 1998). Here is the summary:
How does the law regard and define mental incompetence, when faced with the problem of meting out justice? To what extent has the law relied on extra-legal authorities—be they religious or scientific—to frame its own categories of mental incompetence and madness? Wild Beasts and Idle Humours takes us on an illuminating journey through the changing historical landscape of human nature and offers an unprecedented look at the legal conceptions of insanity from the pre-classical Greek world to the present. Although actual trial records are either totally lacking or incomplete until the eighteenth century, there are other sources from which the insanity defenses can be constructed.
In this book Daniel N. Robinson, a distinguished historian of psychology, pores over centuries of written law, statements by legal commentators, summaries of crimes, and punishments, to glean from these sources an understanding of epochal views of responsibility and competence. From the Greek phrenesis to the Roman notions of furiosus and non compos mentis, from the seventeenth-century witch trials to today’s interpretation of mens rea, Robinson takes us through history and provides the intricate story of how the insanity defense has been construed as a meeting point of the law and those professions that chart human behavior and conduct: namely religion, medicine, and psychology. The result is a rare historical account of “insanity” within Western civilization.
Wild Beasts and Idle Humours will be essential reading for anyone interested in the evolution of thinking not merely about legal insanity but about such core concepts as responsibility, fitness for the rule of law, competence to enter into contracts and covenants, the role of punishments, and the place of experts within the overall juridical context.
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FROM WIKIPEDIA:
Upon moving to become Professor of Clinical Psychiatry at the University of Munich in 1903, Kraepelin increasingly wrote on social policy issues. He was a strong and influential proponent of eugenics and racial hygiene. His publications included a focus on alcoholism, crime, degeneration and hysteria.[12] Kraepelin was convinced that such institutions as the education system and the welfare state, because of their trend to break the processes of natural selection, undermined the Germans’ biological "struggle for survival".[5] He was concerned to preserve and enhance the German people, the Volk, in the sense of nation or race. He appears to have held Lamarckian concepts of evolution, such that cultural deterioration could be inherited. He was a strong ally and promoter of the work of fellow psychiatrist (and pupil and later successor as director of the clinic) Ernst Rudin to clarify the mechanisms of genetic inheritance as to make a so-called "empirical genetic prognosis".[12]
Martin Brune has pointed out that Kraepelin and Rudin also appear to have been ardent advocates of a self-domestication theory, a version of social Darwinism which held that modern culture was not allowing people to be weeded out, resulting in more mental disorder and deterioration of the gene pool. Kraepelin saw a number of "symptoms" of this, such as "weakening of viability and resistance, decreasing fertility, proletarianisation, and moral damage due to "penning up people" [Zusammenpferchung]. He also wrote that "the number of idiots, epileptics, psychopaths, criminals, prostitutes, and tramps who descend from alcoholic and syphilitic parents, and who transfer their inferiority to their offspring, is incalculable". He felt that "the well-known example of the Jews, with their strong disposition towards nervous and mental disorders, teaches us that their extraordinarily advanced domestication may eventually imprint clear marks on the race". Brune states that Kraepelin's nosological system was "to a great deal, built on the degeneration paradigm".[13]
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I believe that Kraepelin's view explains in part why therapeutic nihilism regarding serious mental illness and schizophrenia in particular is still, like a religion, a belief that is held onto despite evidence that persons with serious mental illness, including schizophrenia, do recover.
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I am aware there has not been much research on this subjects despite the Psychologist delivered reflective practice 's popularity within in-patient mental health services.  Sometimes both services and staff feel drained when they have challenging patients within their care in-light of the need for care delivery to be in the best interest of the patient. 
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I am researching the impact on health professionals when a client commits suicide with a view to composing a hospital Trust policy and implementing improved organisational pathways and structures to ensure support for those affected.
I would welcome advice from anyone who has been involved in implementing robust support for professionals in these circumstances and/or composing organisational pathways and policies in this regard.
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Dear Thomas,
Thanks for raising such an important question. Losing a client/patient through suicide is devastating to all involved. Unfortunately it happens quite frequently. Here are some resources to consider:
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does anyone know where i can find recent papers on "close nursing observations in mental health hospitals"?
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Hi Audrey,
it might be helpful when you search to broaden your terms so your net is thrown as wide as possible. In Australia I would include, high dependency, seclusion, specialling   to try and find as many articles as possible.  regards  Lorna
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Is there a validated german translation of the "vestibular disorder activities of daily living scale" (VADL)?   Thank you
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Dear  Colleague,
may I suggest you to ask to  Prof THomas Brandt from Munchen University  in Germany working on the vestibular system: Thomas.Brandt@med.uni-muenchen.de
Sincerly.
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Hello Science-Community,
a few days ago I talked to an occupational therapist about respiratory rates and patterns in children with ADHD. From her experience she is quite sure that children with ADHD usually show abnormal breathing patterns, which does make sense, but I can’t seem to find any reliable studies on it. There are lots of studies on the connection of ADHD and sleep apnea, but none on abnormal breathing in the state of being awake.
Does anyone of you know a study of that kind?
Thank you in advance and have a great day.
Tim
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Hello Tim,
I suggest you to take a look at the paper "Learning disabilities and mouth breathing in subjects with attention deficit hyperactivity disorder diagnosis" published by Vera et al. The study report an association between ADHD and higher rates of mouth breathing, being an interesting discussion subject.
Best Wishes,
Natan
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articles and books relevant to fear in psychiatric patients, especially if there is evidence that compares psychiatric patients and mentally healthy people about the feeling of fear.
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Psychiatric patients is as vague a term as people. Psychiatric patients (meaning people under treatment by a psychiatrist or psychiatry service) spans a vast range of problems.  Indeed, one of the sources of stigma in mental health is the tendency of people to label them all as a single entity. 
My wife, who is a psychiatrist, has just read your question over my shoulder and is very upset by it. Are you suggesting that they are not human in the same way that 'normal' people are human? 
The feeling of fear, too, is a vague term, and I suggest that here, too, you need to clarify your thinking. Fear of specific things (timor in latin) contrasts with a feeling of dread (metu
Where does your question link up with advancing knowledge? What literature have you read? 
More important, what people with mental health problems do you know? And have you talked to them?
As it stands, the question sounds stigmatising and belittling.
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I have been using techniques used in abreaction using IV diazepam to feed my patients with mental illnesses who present with food refusal for days.  It has always produced instant feeding. I am of the opinion that it is a life-saving procedure.  I have always wanted to produce a manual for it and try it in medical conditions as well.  I need any recent developments in this abreaction procedure.
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Rarely used for PTSD  for many reasons, including possibility of creating false memories
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In the case of major depressive disorder treatment (MDD) a full remission is main goal of the treatment, however about 2/3 of patients fail to achieve remission in first year of the treatment with antidepressant. In this point of view achieving remission is often connected with use of 2 different antidepressants (e.g. bupropion and SSRI, trazodone and SSRI, mirtazapine and venlafaxine ... ) or switching. In real clinical practice antipsychotics are also often added (e.g. aripiprazole, quetiapine and olanzapine). 
When you make decision which way (combine or switch) is more appropriate for the patients with MDD?
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This is a huge question and virtually with no simple answer. Partially responsive patients often represent a mixture of biological, psychosocial, personality, addictions and even economic or legal problems. Drugs provide no real benefit then. However, generally speaking, I try to keep treatment simple and prefer multiacting drugs over combinations. What I always try to add are BDNF-related therapies (such as fitness training or yoga:-) and CBT elements.
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In this study I have always been perceived that AIP was the main findings, however when looking at the results again I am not sure if there is an error in the findings or I have been blinded (most likely the latter) to think that AIP has been the main finding of this study but in actual fact PCTis,  where his main finding as far as the results of the urine tests. In his results he states that 4 were positive PBG and 270 positive porphyrins, his final conclusion was that his study found 7 with AIP and 4 with PCT. I hope this makes sense. I am using this study in my thesis.  I have enclosed a copy of the article. Thanks Karen
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1) There were a total of 1774 patients in the survey
2) 4 patients had raised urinary porphobilinogen levels (call it group PBL)
3) 270 patients had raised urinary porphyrin levels (call it group POR)
4) 4 patients had both raised (call it group BOTH)
5) 1774-278=1496 did not have raised levels (call it group NONE)
6) In the 278 patients with raised levels, 7 had AIP (clinically) and 2 had PCT (clinically), but we are not told from which of the above groups each of them came from.
7) we are told that 268 patients from group POR did not have PCT, so presumably 2 did have PCT (as opposed  to AIP)
8) 268 in group POR had alcohol problems, and the authors give three reasons as to why this group had  raised porphyrin levels
So, this survey shows that porphyria is rare  in psychiatric inpatients with a point prevalence of 9/1774 (0.5%) in this survey. The chance of porphyria when there was a positive test result was 9/278 (3.2%, which is the sensitivity of the test ), and the chance of not having porphyria if the test was negative was 1496/1496 (100%, ie the specificity of the test). This survey showed that other factors can raise urinary porphyrin levels.
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I am working with South Australian law but am interested in international law.  Who are the carers?.  What support do they receive?   Have used deontological and utilitarian ethics, where does ethic of care come in?  How can the needs of the patient be balanced with the needs of carers, families and communities?  Stereotyping of the patients and their needs is a  problem. 
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Depending on the quality of the care a person receives, he or she may transform from being 'involuntary' to being 'voluntary'. It doesn't always happen, but many times it does, so it is always worth trying to try one's best to do whatever evidence has shown to be most effective for the majority.
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In last decade this is very important question and this issue should be discussed within each country, unfortunately only some countries have conducted this trials (U.K., U.S.). In many countries there are still no data on this topic. According to the some data available in the literature, patients with mental disorders are very often overtreated and especially antipsychotic polypharmacy is used in 1/3 cases without any evidence to support its use. In many cases appropriate treatment strategy with the use of advanced psychopharmacology and outcomes from the clinical trials can avoid the polypharmacy.
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30 Million Americans Are Victims to Polypharmacy  
Here’s something mind boggling to consider. In the past 10 years, research has shown that the percentage of people over 60 who take five or more medications has jumped from 22 percent to 37 percent. More than 30 million Americans take five or more prescription drugs regularly, often called “polypharmacy.”
Each year, about one-third of seniors experience serious adverse effects as a result of drug interactions, so it’s necessary to be cognizant of the risks and dangers. There are a number of measures a senior can take to avoid the health risks associated with polypharmacy. Observations and tips from Papatya Tankut, vice president, professional pharmacy services, CVS/Pharmacy:
  • Developing a relationship with a pharmacist can help better manage medications and prevent potential and harmful drug interactions.
  • Medication adherence is a growing concern as more Americans neglect to fill prescriptions and take medications as directed.
  • Consult a pharmacist before adding any vitamins or supplements to avoid interactions.
  • If a senior is unsure about a medication or is experiencing a side effect, tell the pharmacist or a trained health expert.
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A patient came to my practice for ongoing and worsening anxiety attacks. No usual interventions were effective. Symptoms led back to time of  Lasik surgery. Although he had 20/20 visual acuity, with haloes and starbursts, there was no relevant feedback about the post operative course. I am familiar with the condition in children and teenagers, but not with these moderating factors. It seems that vision therapy is indicated, but I'm wondering about correlational research with the three conditions.
Thank you.
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To Ann Payne,
Thank you for describing  your clinical observations,  adding to the evidence of this issue.  I believe that the recognition and awareness of the possibility of this condition, needs more research. Since I posed the question, I've been reading the research. In my recent reading and career experience this is "convergence insufficiency" due to muscles not working together. It is a condition that occurs in children and young people without having cataract surgery; vision therapy or specific eye exercises are the treatment of choice. In the past, prism eyeglasses were prescribed. In practice, There are simple strategies for screening.
The front-runner of treatment and research was Dr. Constantine “Gus” Forkiotis, a developmental optometrist, since deceased. His seminal research and publications are worth reading.
Something to consider while taking  the medical history in psychiatric assessment.
Janet
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I am looking at the debate about whether DID exists and whether it is ethical to take the disorder out of the DSM-V.
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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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According to the many well designed trials and reports, there is an important correlation between hypertension and psychiatric disorders. Psychiatric patients are often treated with antihypertensive agents. If we know that treatment with antidepressants and antipsychotics is often long-term we should be very careful, which antihypertensive agent is appropriate for these special patients. These patients are often treated with different specialists and many drug-drug interactions (e.g. indapamide-clozapine) occur within pharmacotherapy.
My opinion with the use of EBM:
- ACE inhibitors should be used first and those with longer half life (especially those with appropriate pharmacokinetics accroding to the kidney failure; e.g. Fosinoprilat). Because psychiatric patients are usually treated with antidepressants (e.g. trazodone) and antipsychotics (e.g. clozapine and quetiapine), which can make hypotension it is very important to use ACE inhibitors with longer half life (to avoid serious short hypotension and falls).
- diuretics (e.g. Indapamide) should be avoided. Although these agents are second line in many international guidelines for hypertension treatment they can incude serious prolongation of QTc, which can have very bad consequences (e.g. death, torsade). We know that many psychiatric patients are treated with those drugs and we can expect additional action, when many 'dangerous' drugs are used together (e.g. TCA, clozapine, quetiapine, amisulpride etc ... ). Instead of diuretics use CA-antagonist for example (e.g. amlodipine, because is cheap and effective).
- sartans are second line treatment (ACE inhibitors first line). However valsartan could be a good idea in patients where Fosinoprilat is not effective and we have psychiatric patients with kidney failure.
- beta-blockers are very useful in these patients, especially where we can avoid polypharmacy (e.g. propranolol for tremor and hypertension) and add additional efficacy (e.g. pindolol in depression and hypertension). However use of these drug should be with great caution especially in the elderly psychiatric patients.
Especially a great caution is required, when used these drugs in patients with ADHD. In these patients avoid of the use of beta blockers because serious hypertension can occur, especially when withdrawal is taking place.
- Moxonidine could be a good option in some patients, however drug drug interactions can be very dangerous. To add moxonidine to ACE inhibitors and CA-antagonists could be a better option as add diuretic indapamide.
- Alpfa blockers are not first line treatment, especially in elderly psychiatric patients. Many DDIs can be very dangerous (e.g. pharmacodynamic) and serious hypotension can occur, when used together with antidepressants and antipsychotics.
If i sum up, it is very important to check all possible DDIs before prescribing. It is also very common that psychiatric agents with its mechanism of action have potential to lower blood pressure and usually in these patients antihypertensive agents can be reduced. However, a cooperation among clinical pharmacists and clinicians can be beneficial for these patients.
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Dear Matej
Thank you for sharing your extensive knowledge and indeed experience in this complicated topic. 
As for treatment of hypertension, HIV, cautious combination (yes I avoid the term polypharmacy) therapy has important role in effective treatment of individuals with psychiatric disorders.
Given the risk of DDIs, its important to have access to all the relevant information.
I use an app (for smart phone) called Epocrates.
Happy to learn about any other useful apps colleagues use.
Rashid 
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In your opinion, What are the five (5) most effective anti depression drugs with their generic and brand names having minimum adverse affects?
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I don't believe antidepressants can be ranked this way.  Among the categories (SSRI, SNRI, SSNRI, Atypical Antidepressants, Tricyclics and MOAIs, one must consider multiple patient variables including comorbidities, other medications they are taking, age of the patient, which is FDA approved for which ages and conditions, specific diagnosis and target symptoms.   Also a careful family history is essential to see if others, particularly first generation relatives, have been treated with one or more antidepressants and how they responded.  The selection of antidepressants is more complex than choosing from a  favorite 5.   
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If yes has there been any effects on the patient's emotions?
If one were to postulate forward then one would expect improvement in mood since as a Substance P antagonist it should have some benefits in lifting depression and or anxiety.
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Mohsain: I have not been reviewing pharmaceuticals recently, but the primary psychiatric drugs ("major psychotropics") that were considered problematic in institutions in the 1970s (e.g., cut back the haldol or take it off) are still in use; the newest drug in that category was respridone (just went generic a few years ago) which resulted in a few years in again the tardive dyskinesia symptoms and neck injury. Believe it or not, sometimes a minor sedative (good night's sleep) or tranquilizer (though potential for misuse) may help to relieve symptoms (e.g., valium to relieve muscle spasms). Many of "our clients" from institutions did much better without the drugs or in the lowest dosages. Good to meet you. Julie Ann Racino  about.me/julieannracino
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Are such associations exclusively determining the individual trigger stimulus?
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I don't understand what you mean be associaitons in this context?
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Has anyone ever seen a finding where people with schizophrenia perform more abnormally (on a cognitive or perceptual task) when stabilizing, compared to when they are acutely psychotic? I just completed a study where it looks like patients perform normally at hospital admission, abnormally at hospital discharge, and then normally again several months later. This doesn't seem to be an artifact (and it is replicated across multiple task conditions) but I have never seen a result like this before. The task is a visual perception task that involves integration of information and then an illusion effect.  Any suggestions will be greatly appreciated! Thanks, Steve
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Sorry I have no study info for you but here are some thoughts. Hospitalization itself can be a very traumatic experience, with true recovery to baseline occurring gradually after discharge. When patients look like they are beginning to recover is when they are released, as long as there is no longer a danger to self or others, or based on individual state laws. And while hospitalized, the patient may be on other PRN meds which are not continued after discharge but serve more to help the patient deal with the stress of a sometimes chaotic psych hospital environment. The last dose is often administered just before discharge. If you or I spent a week locked up in a psych hospital we would probably score poorly on a perceptual task on the day of discharge. Confinement and loss of freedom are disorienting, regardless of how helpful or necessary it may be. I am also wondering if these patients are returning to the same medication regiment prior to hospitalization, or are on a new regiment.
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Does anyone have a daily mood chart which would be helpful for patients with PTSD?
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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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Parents of children with ASD are frequently asking me about oxygen therapy for their children. I need some evidences about the topic. Do you agree using Hyperbaric Oxygen Therapy for autism? is there any evidence about it?
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No. There is no scientific evidence that it can. This is yet another pseudoscientific "cure" for autism that gives false hope to vulnerable, desperate parents.
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I'm working on a paper about reliability of subjective clinical prognosis (but evaluated with different tools than CGI) in patients with first episode schizophrenia, but I don't find any references. Moreover I can't neither  find data about the reliability of subjective clinical prognosis in general in psychiatry. Any help would be more than welcomed! 
Many thanks, Vali. 
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Diagnosis is prognosis- Goodwin & Guze's Psychiatric Diagnosis is the reference for prognosis in psychiatry, as it cites all the longitudinal studies that follow the clinical course of the various psychiatric diagnoses with such studies. There are such longitudinal studies in schizophrenia, and following the clinical course of schizophrenia over time, a distinction is made between good prognosis and bad prognosis, as outlined in the following studies (cited in Psychiatric Diagnosis)http://www.ncbi.nlm.nih.gov/pubmed/12084423 and http://www.ncbi.nlm.nih.gov/pubmed/16098287.
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In the last few years many prescribers do not prescribe IR-MPH in their practice, although clinical guidelines do not support this practice, especially in the titration phase. A pharmaceutical industry is very strong towards newer forms and atomoxetine, which is lower in term of efficacy (effect sizes obtained from meta-analyses). How IR-MPH should be used that patients with ADHD are treated more appropriate? Easy question but hard to answer.
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At the end of the day, despite what treatment guidelines say about what is first line treatment for ADHD, it comes down to cost and value. Industry-sponsored articles from thought leaders in association with industry will not be able to answer this without bias. For patients without the resources to buy more expensive, patented, long-acting medications, then this is an easy answer- MPH-IR is a cost-effective solution. For 3rd-party payers that pay for more expensive, patented, long-acting medications, they should do their own cost-analysis and not be swayed by the biased literature regarding ADHD treatment guidelines.
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According to the many trials and guidelines the use of antipsychotic polypharmacy is not recommended, however more than 1/3 of patients are treated with antipsychotic polypharmacy (APP). Risperidone was often used in many trials and many of them are negative (N Engl J Med. 2006 Feb 2;354(5):472-82.). In last years paliperidone is available, however there is a big lack of studies with APP, where paliperidone is included, although is often used in clincal practice. It is interestingly why these studies have not been conducted yet; if it is because of negative trials with risperidone and 'afraid' or another reasons have been existed.
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It is certainly worth having data on all combinations to guide us.
One reason I sometimes choose other second generation antipsychotics over risperidone (R) and paliperidone (P) is because both cause clinically significant increases in serum prolactin. And as regards hyperprolactinemia, P is worse than R, probably because higher doses of P are required to pass the blood brain barrier...but the pituitary is not 'protected' by the blood brain barrier and is therefore exposed to high levels of P
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What are the cognitive effects of electroconvulsive therapy?
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The technique of the electroshok is necessary for certain patient, on all for those that run risk, the life is in danger that is to say, of other or the one of themselves.  The employment of the electroshock is the most effective means to treat a serious schizophrenia, a depression with ideas suicides or a state of agitation in a bipolar depression. This technique produces a convulsive answer that is minimized with the employment of anesthesia and muscle relaxants. The person doesn't suffer at all but she also brings negative consequences: it can affect the memory, he/she brings harnessed one period confusional, the cognitive processes go in deterioration, all this characteristic of the illness also. Many come the necessity of this technique but other they don't have her.
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Usually the antipsychotics are titrated very fast in first 1-3 weeks. However there are several reasons for non-response and one of them is also 'pharmacokinetic failure', when usually even higher doses are used as recommended. Often, because of non-optimal titration (too fast) patients are treated with high doses to fast and serious adverse event (e.g. EPS) are often occured. Although is known from EBM trials that for optimal effect prescriber should wait smth until 8-12 weeks of monotherapy within the maximal recommended dose, usually in clinical practice doses are too fast titrated and consequences are often seen in antipsychotic polypharmacy, which has not many support in EBM and clinical guidelines for management of schizophrenia. Easy question, however very hard to answer ...
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It would be a good idea to establish if the patient was actually metabolising the drug before titration.  'Pharmacokinetic failure' is frequently associated with the inability of the patient to metabolise the drug and also in an alarming number of cases where the wrong drug is being administered.  
The often cited and utterly unscientific nonesense of 'treatment resistant schizophrenia'  is nothing of the sort.  The reason the patient 'resists' the medication is because it is the wrong medication.  Psychiatrists and psychiatric nurses should be required to complete a full course in pharmacology before being allowed to prescribe. the fact remains that many prescribers have little more than a rudimentary understanding of pharmacokinetics and pharmacodynamics and simply follow the pack when it comes to treatment.
The death rate from faulty prescribing is an alarming testimony to the pharmacological ignorance of many practitioners.
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Psychiatric patients usually take many different medications and often they have been already treated with beta-blockers. However, there are several cases in where You should add beta-blockers, because of newly recognized heart failure or even atrial fibrillation. Often psychiatric patients take medications, which included antipsychotics or even worse an antipsychotic polypharmacy or combinations with antidepressants. According to the survival studies We know that treatment with beta-blockers in patients with stable heart failure (EF less than 35 %) is necessary for better surviving.
The third group of cases consists the consequences of psychotropic medications adverse events (e. g. arrhythmias and clozapine or olanzapine) or prolonged QTc and supraventricular arrhythmias (e. g. amisulpride with clozapine combination or ziprasidone use and escitalopram together). In these cases a trial with beta blockers is usually a first step before drug discontinuation.
From EBM we know that combination of clozapine and amisulpride is benefitial in short term trials, however long term use should lead to several complications in this field.
To sum up, DDIs with psychotropics and beta-blockers should be calculated before prescribing beta-blockers. For example, atenolol is not appropriate with several antipsychotics and antidepressants (QTc prolongation). Also story with metoprolol is more or less the same, however metoprolol is very selective for B1 receptors, however there are cases of induced delirium with propranolol. Smart use included pindolol, especially in patients on antidepressants, because of add on efficacy, however we do not have long term trials.  At the end I think cooperation between clinical pharmacist and psychiatrist and cardiologist is the best approach to deal with these patients.
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I prescribe Inderal (propranolol) in consultation with internists/cardiologists for treatment of lithium tremor and occasionally performance anxiety. Others (e.g., Yudosky and Silver) have published extensively on using high dose propranolol for rage attacks in persons with TBI.  Other than that, I do not prescribe beta blockers.
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Nitrofurantoin (NF)-induced adverse effects have been reported frequently, although NF seems to be a first line treatment for lower urinary infections according to the last E.U. and U.S. guidelines. However its use in psychiatric patients should be reviewed with a great caution. In these cases the use of penicillin is therefore sometimes more appropriate, although the total antibiotic consumption rises. Because of NF use, a dose adjustment because of its adverse events (hallucinations) is also possible and cooperation with clinical pharmacist is beneficial in these cases. What do you think?
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This is true Dr.stuhec
Nitrofurantoin should be avoided in geriatric patients in general not only in psychiatric patients.
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Antipsychotic polypharmacy refers to the co-prescription of more than one antipsychotic drug for an individual patient. According to the many studies consumption of clozapine in patients with chronic schizophrenia is still low (about 25 %) and antipsychotic polypharmacy prevalence before clozapine use is very high, although the evidence usually does not support its use. How to manage patients with chronic schizophrenia with higher clozapine consumption?
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Hi Matec,
Polypharmacy in psychosis is ill-adviced. It is associated with high rates of morbidity and increase in mortality. Clozapine mono therapy should probably be used more often. Also, note a recent study on the American Journal of Psychiatry by Petrifies et al. regarding the concurrent use of clozapine and electroconvulsive therapy for clozapine-resistant schizophrenia where excellent results were found (Petrides G, Malur C, Braga RJ, Bailine SH, Schooler NR, Malhotra AK, Kane JM,
Sanghani S, Goldberg TE, John M, Mendelowitz A. Electroconvulsive therapy
augmentation in clozapine-resistant schizophrenia: a prospective, randomized
study. Am J Psychiatry. 2015 Jan;172(1):52-8. doi:
10.1176/appi.ajp.2014.13060787. Epub 2014 Oct 31. PubMed PMID: 25157964)
Best regards,
Fidel
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It looks to me that the relationship between anxiety and dementia is much less strong than the one between depressive symptoms and dementia. And that anxiety could be confounded by depression (and vice-versa?).
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I refer to: tendencies to omnipotent thought; avoidance of otherness; Immediate drive discharge ecc.
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 there is a most excellent tool - severely mistrusted by our evidence-debased friends, apparently - called an analyst.
This "tool" is able to use listening, intelligence, feeling, intuition, compassion and 100 years of psychoanalytic theory to fairly accurately predict and "measure" and to understand the degree and nature of regression in a particular person.
It is an expensive tool - little understood by the evidence-debased CBT-government health-fund alliance - but, it works. And updates are free, but require ongoing genuine interest in the human psyche and the world of the unconscious. To purchase a license requires great patience and curiosity and a mistrust of the usual forms of "evidence".
 That is the shortest answer that I can give.
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Dear all,
Please, which are the most commonly used clinical cut-offs for considering depression in the following depression scales?
GDS- 15 items version
HADS- 7 items version (Depression sub-scale)
MDRS- 10 items version
Cornell
thanks so much
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See the following link for MADRS cut-off
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Hello, 
I'm trying to understand if psuchiatric satisfaction scale for inpatient are commonly and routinely used in the acute psichiatric unit.
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I believe the NHS has implemented the 'friends and family' test as a means of measuring satisfaction with inpatient services
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I have read studies that discuss mood and color in psychiatric settings, but often the study is of a person and the color which does not take into account the many other variables experienced by someone in the emergency department.  There are studies of other rooms, such as used during therapy or in the general milieu.
I'm looking specifically for door color since our rooms are and will always be laboratory white.  I'm thinking that a great study would be to have at least two rooms with different colored doors and see which one the person (in acute psychiatric distress) chooses indicating a perception of safety.
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Lavender (the herb) has been shown to have calming effects on children at night time. Now modern designers are using the color extensively in designing bedrooms to exude an atmosphere of serenity in the bedroom of adults.  The paint distributor company Behr makes a color called "Calm Retreat" which is a very light Lavender. Depending on the lighting in the room, it changes color variations;but in any case it is very subtle and a wonderfully calming shade appropriate for doors and offices.
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Does anyone have any views on a biological basis for PTSD? C-reactive protein (CRP) a marker in inflammation has been associated with combat related PTSD in soldiers. Biological factors in chronic psychiatric illness have been elusive but this might give us an insight into why some people are more negatively responsive to stress than others.
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As others have mentioned, there are genetic polymorphisms that can make one more vulnerable to PTSD, but you don't necessarily need to have these differences to develop PTSD.
Here's how I wrap my head around this type of genetic/environment interaction situation. Stay with me, I swear I'll connect it :). Wine. Grapes are the best fruit to make wine with; the natural properties of grapes allow the fruit to create wine without any additives during the fermentation process. However, wine can be made without grapes... it can be made with all sorts of fruit and even rice, but these materials are not as easily converted into wine and require special additives and/or processes during fermentation.
In this illustration, wine is PTSD; grapes are the serotonin transporter genes with one or two shorter alleles. The other types of fruit and the rice are the genes with the long alleles, they can make wine (develop PTSD) but it's easier with the grapes (shorter alleles). That being said, just because you have grapes (short alleles) doesn't necessarily mean you are going to make wine (develop PTSD), you could always have a nice fruit salad. :)
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In addition to environmental intervention, behavioral management, carer skills adjustments, what would be an effective medication for hypersexuality or inappropriate sexual behaviors in elderly patients with neurocognitive disorders? 
Some research on the topic:
Inappropriate sexual behaviors in cognitively impaired older individuals. Am J Geriatr Pharmacother. 2008 Dec;6(5):269-88.
Hypersexual behavior in frontotemporal dementia: a comparison with early-onset Alzheimer's disease. Arch Sex Behav. 2013 Apr;42(3):501-9.
Rivastigmine in the treatment of hypersexuality in Alzheimer disease. Alzheimer Dis Assoc Disord. 2013 Jul-Sep;27(3):287-8. 
Different classes of medication have been suggested to be effective, such as TCAs, SSRIs, antipsychotics, estrogens, anti-androgens, and LHRH agonists, etc. However, currently there is  lack of consensus as to what would be the most effective pharmacotherapy. And there would be substantial individual differences between different patients. If anyone has the experience of treating hypersexuality or inappropriate sexual behavior, could you share the clinical experience and make some comments on its pharmacotherapy? Are there differences in terms of pharmacotherapy when treating male or female patients with hypersexuality?
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Dear Chen-Chia,
DEPENDS -- on the "cause" . . . Several years (decades) ago, my wife and I were invited to present at a symposium for elderly patients at a major psychiatric hospital. As we were both giving keynote addresses, we were invited on grand rounds. 
One of the patients we encountered was an elderly man, a grandfather, who although he had developed Alzheimer's was reasonably well adjusted and living at home with his son's family. Everyone loved and helped care for "grandpa" until he started making unwarranted sexual comments and advances towards his two grand-daughters. Subsequently, several weeks before we met him, he was transferred to the long-term psychogeriatric ward of the hospital -- for permanent stay.
Given his history, symptomatology, and the fact that we were both lecturing on the effects of medication use among the elderly, we suggested that his inappropriate behaviour might be due to a cyanocobalamin (vitamin B12) deficiency. A Shillings test revealed that his B12 level of extremely below normal. Subsequent daily injectable doses of 1000 mcg per day resulted in significant improvement in his mental status by the end of several weeks AND after several months, he was happily reunited with his family.
A true story, with a happy ending, that we also reported on as a case history at that time in the medical literature (see my list of publications for the exact reference). This response does NOT detract from the excellent advice that our other 2 colleagues have already provided you with. BUT, it should ADD to that advice and be a reminder to all of us clinicians that the first and most common response is not always the best for a particular individual patient . . .
I hope that this response is of some assistance.
Sincerely,
Lou
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I am interested in knowing more about the endurance of anhedonia in BPD patients after they have suffered a depression. I can't find relevant literature on this topic, so perhaps someone here can help me out?
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Consider iatrogenic etiologies secondary to either dopamine antagonists or SSRIs.
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would someone like to share some articles about it?
- about the effectiveness of antidepressant (both prove and reject)
- about the side-effects of antidepressant
- qualitative research of the patient after taking antidepressant
- others articles you think is related to the question
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You are the crafter/creator of your life.
Human life is a journey of relationships:  Love & Work & Awe
Daily health is mediated by:  diet & exercise & sleep
Illness is treated with medical technology and technique.
Medicine is one tool to treat illness
so that
You can return to life.
As the research cited above shows, medicine has worked for some.
If you are debilitated and apart from your human life journey, use the tools of medicine.
You